miR-524-5p of the primate-specific C19MC miRNA cluster targets TP53IPN1- and EMT-associated genes to regulate cellular reprogramming
Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate...
Uloženo v:
| Vydáno v: | Stem cell research & therapy Ročník 8; číslo 1; s. 214 - 15 |
|---|---|
| Hlavní autoři: | , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
BioMed Central
29.09.2017
BioMed Central Ltd Springer Nature B.V BMC |
| Témata: | |
| ISSN: | 1757-6512, 1757-6512 |
| On-line přístup: | Získat plný text |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | Background
Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process.
Methods
A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR.
Results
Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4.
Conclusions
Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. |
|---|---|
| AbstractList | Abstract Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process. Methods A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR. Results Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4. Conclusions Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process. Methods A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR. Results Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4. Conclusions Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to 'reprogram' somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process. Methods A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR. Results Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4. Conclusions Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. Keywords: C19MC, miR-524-5p, Reprogramming efficiency, Cell proliferation, Apoptosis, Pluripotency genes, MET, TP53INP1, ZEB2, SMAD4 Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process. Methods A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR. Results Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4. Conclusions Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to 'reprogram' somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process. A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR. Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4. Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR. Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4. Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to 'reprogram' somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process.BACKGROUNDIntroduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to 'reprogram' somatic cells to become induced pluripotent stem cells (iPSCs). Several microRNAs (miRNAs) are known to enhance reprogramming efficiency when co-expressed with the OSKM factors. The primate-specific chromosome 19 miRNA cluster (C19MC) is essential in primate reproduction, development, and differentiation. miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). This study aimed to elucidate possible contributions of miR-524-5p to the reprogramming process.A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR.METHODSA miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies that stained positively with alkaline phosphatase (AP) and Nanog were quantified to determine reprogramming efficiency. A miR-524-5p mimic was transfected to MSCs to investigate the effects of miR-524-5p on TP53INP1, ZEB2, and SMAD4 expression by real-time polymerase chain reaction (PCR) and Western blot. Direct gene targeting was confirmed by luciferase activity. A phylogenetic tree of TP53INP1 was constructed by the Clustal method. Contribution of miR-524-5p to cell proliferation and apoptosis was examined by cell counts, BrdU, MTT, and cell death assays, and pluripotency gene expression by real-time PCR.Co-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4.RESULTSCo-expressing the miR-524 precursor with OSKM resulted in a two-fold significant increase in the number of AP- and Nanog-positive ESC-like colonies, indicating a role for miR-524-5p in reprogramming. The putative target, TP53INP1, showed an inverse expression relationship with miR-524-5p; direct TP53INP1 targeting was confirmed in luciferase assays. miR-524-5p-induced TP53INP1 downregulation enhanced cell proliferation, suppressed apoptosis, and upregulated the expression of pluripotency genes, all of which are critical early events of the reprogramming process. Interestingly, the TP53INP1 gene may have co-evolved late with the primate-specific miR-524-5p. miR-524-5p also promoted mesenchymal-to-epithelial transition (MET), a required initial event of reprogramming, by directly targeting the epithelial-to-mesenchymal transition (EMT)-related genes, ZEB2 and SMAD4.Via targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions.CONCLUSIONSVia targeting TP53INP1, ZEB2, and SMAD4, miR-524-5p contributes to the early stage of inducing pluripotency by promoting cell proliferation, inhibiting apoptosis, upregulating expression of pluripotency genes, and enhancing MET. Other C19MC miRNAs may have similar reprogramming functions. |
| ArticleNumber | 214 |
| Audience | Academic |
| Author | Nguyen, Phan Nguyen Nhi Sugii, Shigeki Choo, Kong Bung Cheong, Soon Keng Kamarul, Tunku Huang, Chiu-Jung |
| Author_xml | – sequence: 1 givenname: Phan Nguyen Nhi surname: Nguyen fullname: Nguyen, Phan Nguyen Nhi organization: Centre for Stem Cell Research, Universiti Tunku Abdul Rahman, Department of Preclinical Sciences, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman – sequence: 2 givenname: Kong Bung orcidid: 0000-0002-0880-7867 surname: Choo fullname: Choo, Kong Bung email: chookb@utar.edu.my organization: Centre for Stem Cell Research, Universiti Tunku Abdul Rahman, Department of Preclinical Sciences, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman – sequence: 3 givenname: Chiu-Jung surname: Huang fullname: Huang, Chiu-Jung organization: Department of Animal Science, Chinese Culture University, Graduate Institute of Biotechnology, Chinese Culture University – sequence: 4 givenname: Shigeki surname: Sugii fullname: Sugii, Shigeki organization: Singapore BioImaging Consortium AStar, Duke-NUS Graduate Medical School – sequence: 5 givenname: Soon Keng surname: Cheong fullname: Cheong, Soon Keng organization: Centre for Stem Cell Research, Universiti Tunku Abdul Rahman, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Sungai Long – sequence: 6 givenname: Tunku surname: Kamarul fullname: Kamarul, Tunku organization: Tissue Engineering Group, National Orthopaedic Centre of Excellence for Research and Learning, Department of Orthopaedic Surgery, Faculty of Medicine, University of Malaya |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28962647$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9k8Fu1DAQhiNUREvpA3BBlpAQHFJiO7HjC9JqVWCltlRlOVtex866SuLFdhDceXBmuy1sKiBRktH4-_-MR56n2cHgB5Nlz3FxinHN3kZMSc3zAsPDGMvpo-wI84rnrMLkYC8-zE5ivCngorQoWPkkOyS1YISV_Cj72bvrvCJlXm2QtyitDdoE16tk8rgx2lmn0RyLizkC8HKGdDfGZAJKKrQmRbS8quji6hLnSA0NOrtY5ipGrx0YNKg1g4koeRRMO3aQQtp0HUQBMpvg26D63g3ts-yxVV00J3ff4-zL-7Pl_GN-_unDYj47zzWnZcptzWttBS40w5rrUle1Uo0RTFhRVyuuhKohLEXFeEkY14rb0hih8arC3Db0OFvsfBuvbuTtPsMP6ZWTtwkfWqlCcrozEkRCCMzgTUsseF1gigmntMa2aBgHr3c7r8246k2jzZCC6iam05XBrWXrv8mKEQLlgMHrO4Pgv44mJtm7uO2PGowfo8SirAgpMSGAvnyA3vgxDNCqLcWhQsHxH6pVsAE3WA__1VtTOasKLgqKeQ3U6V8ouBvTOw1HzDrITwRvJgJgkvmeWjXGKBefr6fsqz12bVSX1tF3Y3J-iFPwxX73frft_mACwHeADj7GYKzULqmtD5TrOokLuZ0CuZsCCVMgt1MgKSjxA-W9-f80ZKeJwA6tCXsN_qfoF-4DEsE |
| CitedBy_id | crossref_primary_10_1007_s12015_018_9861_6 crossref_primary_10_1093_biolre_ioz022 crossref_primary_10_1186_s12935_018_0612_1 crossref_primary_10_1038_s41467_022_30775_w crossref_primary_10_3389_fgene_2024_1389558 crossref_primary_10_1038_s41598_020_59812_8 crossref_primary_10_3389_fcell_2025_1593207 crossref_primary_10_1007_s00401_020_02182_2 crossref_primary_10_1016_j_dld_2018_03_026 crossref_primary_10_1002_cam4_3473 crossref_primary_10_1007_s12015_023_10621_2 crossref_primary_10_3389_fgene_2018_00706 crossref_primary_10_3390_jdb12010001 crossref_primary_10_3390_pharmaceutics14020317 crossref_primary_10_4103_jcrt_jcrt_364_21 crossref_primary_10_1007_s13577_020_00364_4 crossref_primary_10_1016_j_mrfmmm_2024_111872 crossref_primary_10_1186_s12929_018_0461_1 crossref_primary_10_3390_cancers16203537 crossref_primary_10_1016_j_neo_2020_10_009 crossref_primary_10_1089_cbr_2019_3046 crossref_primary_10_3390_genes14071434 crossref_primary_10_1038_s41366_019_0450_9 |
| Cites_doi | 10.1128/MCB.13.5.2919 10.1038/onc.2010.183 10.1038/nature10761 10.1038/emboj.2011.2 10.1016/j.stem.2011.05.001 10.1016/j.celrep.2013.05.027 10.1016/j.semcdb.2014.05.017 10.1002/stem.1149 10.1002/pros.21412 10.1038/nrg3473 10.3389/fcell.2015.00002 10.1016/j.canlet.2015.01.030 10.1089/scd.2009.0426 10.7150/ijms.8356 10.1007/s40268-014-0064-6 10.1186/s12929-017-0326-z 10.1002/stem.1278 10.1158/1541-7786.MCR-11-0421 10.1530/JME-11-0189 10.1016/j.stem.2009.10.007 10.1093/nar/gkq850 10.1186/1471-2407-11-425 10.1038/ncb2366 10.1038/nature05939 10.1016/j.cell.2006.07.024 10.1038/nbt.1862 10.1016/j.stem.2008.08.014 10.1038/cdd.2014.28 10.1016/j.stem.2011.03.001 10.1038/ncb2613 10.3389/fgene.2013.00080 10.1038/nrc3318 10.1038/nrg2955 10.1002/jcp.24104 10.1016/j.compbiolchem.2010.08.001 10.1093/nar/gkp205 10.1038/ncb1827 10.1186/1471-2164-8-166 10.1074/jbc.M301979200 10.1074/jbc.M601811200 10.1038/srep03852 10.1016/j.scr.2014.03.007 10.1093/neuonc/not162 10.1016/j.stem.2010.11.010 10.18632/oncotarget.2559 10.1016/j.molcel.2012.01.020 10.1016/j.stemcr.2015.02.009 10.1038/nrm3758 10.1073/pnas.1212769110 10.1038/cdd.2012.30 |
| ContentType | Journal Article |
| Copyright | The Author(s). 2017 COPYRIGHT 2017 BioMed Central Ltd. Copyright BioMed Central 2017 |
| Copyright_xml | – notice: The Author(s). 2017 – notice: COPYRIGHT 2017 BioMed Central Ltd. – notice: Copyright BioMed Central 2017 |
| DBID | C6C AAYXX CITATION CGR CUY CVF ECM EIF NPM ISR 3V. 7X7 7XB 88E 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FYUFA GHDGH GNUQQ HCIFZ K9. LK8 M0S M1P M7P PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS 7X8 5PM DOA |
| DOI | 10.1186/s13287-017-0666-3 |
| DatabaseName | Springer Nature OA Free Journals CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Gale In Context: Science ProQuest Central (Corporate) Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central Natural Science Collection ProQuest One ProQuest Central Proquest Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Biological Sciences ProQuest Health & Medical Collection Medical Database Biological Science Database ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic (retired) ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Biological Science Collection ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | Publicly Available Content Database MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: PIMPY name: Publicly Available Content Database url: http://search.proquest.com/publiccontent sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 1757-6512 |
| EndPage | 15 |
| ExternalDocumentID | oai_doaj_org_article_9c1999161993419780131273381f0d67 PMC5622517 A507903178 28962647 10_1186_s13287_017_0666_3 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GeographicLocations | United States--US |
| GeographicLocations_xml | – name: United States--US |
| GrantInformation_xml | – fundername: FRGS/2/2014/SKK01/UTAR/01/2 grantid: FRGS/2/2014/SKK01/UTAR/01/2 – fundername: HIR-MoE grantid: UM.C/625/1/HIR/MOHE/CHAN/03 – fundername: ; grantid: FRGS/2/2014/SKK01/UTAR/01/2 – fundername: ; grantid: UM.C/625/1/HIR/MOHE/CHAN/03 |
| GroupedDBID | --- 0R~ 53G 5VS 7X7 88E 8FE 8FH 8FI 8FJ AAFWJ AAJSJ AASML ABDBF ABUWG ACGFS ACIHN ACJQM ACPRK ACUHS ADBBV ADUKV AEAQA AENEX AFKRA AFPKN AHBYD AHMBA AHYZX ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIAM AOIJS BAPOH BAWUL BBNVY BCNDV BENPR BFQNJ BHPHI BMC BPHCQ BVXVI C6C CCPQU DIK E3Z EBD EBLON EBS EJD EMOBN ESX F5P FYUFA GROUPED_DOAJ GX1 H13 HCIFZ HMCUK HYE IAO IEA IHR IHW INH INR ISR ITC KQ8 LK8 M1P M7P M~E O5R O5S OK1 P2P PGMZT PHGZM PHGZT PIMPY PJZUB PPXIY PQGLB PQQKQ PROAC PSQYO PUEGO RBZ ROL RPM RSV SBL SOJ SV3 TUS UKHRP AAYXX AFFHD CITATION -56 -5G -BR 3V. ACRMQ ADINQ ALIPV C24 CGR CUY CVF ECM EIF NPM 7XB 8FK AHSBF AZQEC DWQXO GNUQQ K9. PKEHL PQEST PQUKI PRINS 7X8 5PM |
| ID | FETCH-LOGICAL-c734t-f878cf910c61c7c4c58aade969f985b7a9a89f9495674267ca7f4ee9c1b517fd3 |
| IEDL.DBID | RSV |
| ISICitedReferencesCount | 29 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000412195400018&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1757-6512 |
| IngestDate | Fri Oct 03 12:52:24 EDT 2025 Tue Nov 04 01:41:13 EST 2025 Thu Oct 02 12:03:01 EDT 2025 Tue Oct 21 12:46:21 EDT 2025 Tue Nov 11 10:28:48 EST 2025 Tue Nov 04 17:45:07 EST 2025 Thu Nov 13 15:24:43 EST 2025 Thu May 22 21:14:34 EDT 2025 Wed Feb 19 02:41:23 EST 2025 Sat Nov 29 01:46:10 EST 2025 Tue Nov 18 21:30:03 EST 2025 Sat Sep 06 07:28:31 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | Cell proliferation miR-524-5p Pluripotency genes ZEB2 SMAD4 C19MC Reprogramming efficiency TP53INP1 MET Apoptosis |
| Language | English |
| License | Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c734t-f878cf910c61c7c4c58aade969f985b7a9a89f9495674267ca7f4ee9c1b517fd3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| ORCID | 0000-0002-0880-7867 |
| OpenAccessLink | https://link.springer.com/10.1186/s13287-017-0666-3 |
| PMID | 28962647 |
| PQID | 1947934971 |
| PQPubID | 2040189 |
| PageCount | 15 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_9c1999161993419780131273381f0d67 pubmedcentral_primary_oai_pubmedcentral_nih_gov_5622517 proquest_miscellaneous_1945224122 proquest_journals_1947934971 gale_infotracmisc_A507903178 gale_infotracacademiconefile_A507903178 gale_incontextgauss_ISR_A507903178 gale_healthsolutions_A507903178 pubmed_primary_28962647 crossref_citationtrail_10_1186_s13287_017_0666_3 crossref_primary_10_1186_s13287_017_0666_3 springer_journals_10_1186_s13287_017_0666_3 |
| PublicationCentury | 2000 |
| PublicationDate | 2017-09-29 |
| PublicationDateYYYYMMDD | 2017-09-29 |
| PublicationDate_xml | – month: 09 year: 2017 text: 2017-09-29 day: 29 |
| PublicationDecade | 2010 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England |
| PublicationTitle | Stem cell research & therapy |
| PublicationTitleAbbrev | Stem Cell Res Ther |
| PublicationTitleAlternate | Stem Cell Res Ther |
| PublicationYear | 2017 |
| Publisher | BioMed Central BioMed Central Ltd Springer Nature B.V BMC |
| Publisher_xml | – name: BioMed Central – name: BioMed Central Ltd – name: Springer Nature B.V – name: BMC |
| References | J Zhang (666_CR46) 2014; 7 F Jiang (666_CR47) 2011; 11 Y Buganim (666_CR2) 2013; 14 H Hermeking (666_CR49) 2012; 12 K Takahashi (666_CR1) 2006; 126 C Chen (666_CR23) 2005; 33 TR Leonardo (666_CR5) 2012; 14 B Feng (666_CR51) 2009; 11 F Itoh (666_CR29) 2014; 32 D Ye (666_CR41) 2012; 30 KB Choo (666_CR21) 2014; 11 S Lamouille (666_CR54) 2014; 15 S Peuget (666_CR32) 2014; 21 X He (666_CR11) 2014; 9 Z Li (666_CR42) 2011; 30 DA Robinton (666_CR26) 2012; 481 SL Lin (666_CR40) 2011; 39 K Plath (666_CR4) 2011; 12 Y Wang (666_CR13) 2013; 4 VK Singh (666_CR25) 2015; 3 D Hockemeyer (666_CR22) 2008; 3 Y Ishihara (666_CR24) 2014; 14 K Kapinas (666_CR27) 2013; 228 CJ Jung (666_CR28) 2012; 10 N Mah (666_CR37) 2011; 6 V Vaira (666_CR20) 2012; 49 L David (666_CR3) 2014; 12 Y Liang (666_CR18) 2007; 8 PN Nguyen (666_CR7) 2017; 24 S Lin (666_CR17) 2010; 34 K Woltjen (666_CR30) 2009; 5 T Spence (666_CR19) 2014; 16 F Anokye-Danso (666_CR9) 2011; 8 M Li (666_CR50) 2012; 46 D Subramanyam (666_CR14) 2011; 29 W Shi (666_CR53) 2006; 281 S Tsuno (666_CR15) 2014; 4 R Tomasini (666_CR48) 2003; 278 Z Zhang (666_CR39) 2015; 4 N Miyoshi (666_CR8) 2011; 8 S Giusiano (666_CR45) 2012; 72 R Puca (666_CR31) 2010; 29 F Liu (666_CR36) 2015; 359 S Hu (666_CR10) 2013; 31 P Tsukerman (666_CR38) 2014; 5 G Wang (666_CR12) 2013; 110 B Stadler (666_CR6) 2010; 19 L He (666_CR34) 2007; 447 S Ma (666_CR35) 2010; 7 YJ Choi (666_CR33) 2011; 13 M Seillier (666_CR43) 2012; 19 BA Hosler (666_CR52) 1993; 13 ML Bortolin-Cavaille (666_CR16) 2009; 37 J Shahbazi (666_CR44) 2013; 4 21490602 - Nat Biotechnol. 2011 May;29(5):443-8 16714766 - J Biol Chem. 2006 Aug 18;281(33):23319-25 22622027 - Mol Cancer Res. 2012 Jul;10 (7):979-91 24458129 - Sci Rep. 2014 Jan 24;4:3852 20870751 - Nucleic Acids Res. 2011 Feb;39(3):1054-65 24910449 - Semin Cell Dev Biol. 2014 Aug;32:98-106 24556840 - Nat Rev Mol Cell Biol. 2014 Mar;15(3):178-96 19896434 - Cell Stem Cell. 2009 Nov 6;5(5):457-8 23136034 - Stem Cells. 2013 Feb;31(2):259-68 12851404 - J Biol Chem. 2003 Sep 26;278(39):37722-9 28270145 - J Biomed Sci. 2017 Mar 7;24(1):20 22258608 - Nature. 2012 Jan 18;481(7381):295-305 16904174 - Cell. 2006 Aug 25;126(4):663-76 20128659 - Stem Cells Dev. 2010 Jul;19(7):935-50 22552993 - J Cell Physiol. 2013 Jan;228(1):9-20 21970405 - BMC Cancer. 2011 Oct 05;11:425 8474450 - Mol Cell Biol. 1993 May;13(5):2919-28 19339516 - Nucleic Acids Res. 2009 Jun;37(10):3464-73 24311633 - Neuro Oncol. 2014 Jan;16(1):62-71 21285944 - EMBO J. 2011 Mar 2;30(5):823-34 21415849 - Nat Rev Genet. 2011 Apr;12(4):253-65 23131918 - Nat Cell Biol. 2012 Nov;14(11):1114-21 22020437 - Nat Cell Biol. 2011 Oct 23;13(11):1353-60 25633840 - Cancer Lett. 2015 Apr 10;359(2):288-98 24735951 - Stem Cell Res. 2014 May;12(3):754-61 19136965 - Nat Cell Biol. 2009 Feb;11(2):197-203 20863765 - Comput Biol Chem. 2010 Aug;34(4):232-41 17554337 - Nature. 2007 Jun 28;447(7148):1130-4 21112564 - Cell Stem Cell. 2010 Dec 3;7(6):694-707 25699255 - Front Cell Dev Biol. 2015 Feb 02;3:2 16314309 - Nucleic Acids Res. 2005 Nov 27;33(20):e179 21909390 - PLoS One. 2011;6(8):e24351 23386720 - Proc Natl Acad Sci U S A. 2013 Feb 19;110(8):2858-63 25426550 - Oncotarget. 2014 Dec 15;5(23 ):12141-50 23717325 - Front Genet. 2013 May 13;4:80 23681063 - Nat Rev Genet. 2013 Jun;14(6):427-39 22696098 - Stem Cells. 2012 Aug;30(8):1645-54 20514025 - Oncogene. 2010 Aug 5;29(31):4378-87 21620789 - Cell Stem Cell. 2011 Jun 3;8(6):633-8 24608790 - Cell Death Differ. 2014 Jul;21(7):1107-18 22387025 - Mol Cell. 2012 Apr 13;46(1):30-42 17565689 - BMC Genomics. 2007 Jun 12;8:166 25249788 - Int J Med Sci. 2014 Sep 13;11(11):1201-7 23831024 - Cell Rep. 2013 Jul 11;4(1):99-109 25801506 - Stem Cell Reports. 2015 Apr 14;4(4):645-57 22898542 - Nat Rev Cancer. 2012 Sep;12(9):613-26 24551280 - Int J Clin Exp Pathol. 2014 Jan 15;7(2):602-10 24740298 - PLoS One. 2014 Apr 16;9(4):e95213 21538421 - Prostate. 2012 Feb 1;72(2):117-28 22421968 - Cell Death Differ. 2012 Sep;19(9):1525-35 22767050 - J Mol Endocrinol. 2012 Jul 26;49(2):115-24 18786421 - Cell Stem Cell. 2008 Sep 11;3(3):346-353 21474102 - Cell Stem Cell. 2011 Apr 8;8(4):376-88 25303886 - Drugs R D. 2014 Dec;14 (4):253-64 |
| References_xml | – volume: 13 start-page: 2919 year: 1993 ident: 666_CR52 publication-title: Mol Cell Biol. doi: 10.1128/MCB.13.5.2919 – volume: 29 start-page: 4378 year: 2010 ident: 666_CR31 publication-title: Oncogene. doi: 10.1038/onc.2010.183 – volume: 481 start-page: 295 year: 2012 ident: 666_CR26 publication-title: Nature. doi: 10.1038/nature10761 – volume: 30 start-page: 823 year: 2011 ident: 666_CR42 publication-title: EMBO J. doi: 10.1038/emboj.2011.2 – volume: 8 start-page: 633 year: 2011 ident: 666_CR8 publication-title: Cell Stem Cell. doi: 10.1016/j.stem.2011.05.001 – volume: 7 start-page: 602 year: 2014 ident: 666_CR46 publication-title: Int J Clin Exp Pathol. – volume: 4 start-page: 99 year: 2013 ident: 666_CR13 publication-title: Cell Rep doi: 10.1016/j.celrep.2013.05.027 – volume: 32 start-page: 98 year: 2014 ident: 666_CR29 publication-title: Semin Cell Dev Biol. doi: 10.1016/j.semcdb.2014.05.017 – volume: 30 start-page: 1645 year: 2012 ident: 666_CR41 publication-title: Stem Cells. doi: 10.1002/stem.1149 – volume: 9 year: 2014 ident: 666_CR11 publication-title: PLoS One. – volume: 72 start-page: 117 year: 2012 ident: 666_CR45 publication-title: Prostate. doi: 10.1002/pros.21412 – volume: 14 start-page: 427 year: 2013 ident: 666_CR2 publication-title: Nat Rev Gene. doi: 10.1038/nrg3473 – volume: 3 start-page: 2 year: 2015 ident: 666_CR25 publication-title: Front Cell Dev Biol. doi: 10.3389/fcell.2015.00002 – volume: 359 start-page: 288 year: 2015 ident: 666_CR36 publication-title: Cancer Lett. doi: 10.1016/j.canlet.2015.01.030 – volume: 19 start-page: 935 year: 2010 ident: 666_CR6 publication-title: Stem Cells Dev. doi: 10.1089/scd.2009.0426 – volume: 11 start-page: 1201 year: 2014 ident: 666_CR21 publication-title: Int J Med Sci. doi: 10.7150/ijms.8356 – volume: 33 year: 2005 ident: 666_CR23 publication-title: Nucleic Acids Res. – volume: 14 start-page: 253 year: 2014 ident: 666_CR24 publication-title: Drugs RD. doi: 10.1007/s40268-014-0064-6 – volume: 24 start-page: 20 year: 2017 ident: 666_CR7 publication-title: J Biomed Sci. doi: 10.1186/s12929-017-0326-z – volume: 31 start-page: 259 year: 2013 ident: 666_CR10 publication-title: Stem Cells. doi: 10.1002/stem.1278 – volume: 10 start-page: 979 year: 2012 ident: 666_CR28 publication-title: Mol Cancer Res. doi: 10.1158/1541-7786.MCR-11-0421 – volume: 6 year: 2011 ident: 666_CR37 publication-title: PLoS One. – volume: 49 start-page: 115 year: 2012 ident: 666_CR20 publication-title: J Mol Endocrinol. doi: 10.1530/JME-11-0189 – volume: 5 start-page: 457 year: 2009 ident: 666_CR30 publication-title: Cell Stem Cell doi: 10.1016/j.stem.2009.10.007 – volume: 39 start-page: 1054 year: 2011 ident: 666_CR40 publication-title: Nucleic Acids Res. doi: 10.1093/nar/gkq850 – volume: 11 start-page: 425 year: 2011 ident: 666_CR47 publication-title: BMC Cancer. doi: 10.1186/1471-2407-11-425 – volume: 13 start-page: 1353 year: 2011 ident: 666_CR33 publication-title: Nat Cell Biol doi: 10.1038/ncb2366 – volume: 447 start-page: 1130 year: 2007 ident: 666_CR34 publication-title: Nature. doi: 10.1038/nature05939 – volume: 126 start-page: 663 year: 2006 ident: 666_CR1 publication-title: Cell. doi: 10.1016/j.cell.2006.07.024 – volume: 29 start-page: 443 year: 2011 ident: 666_CR14 publication-title: Nat Biotechnol. doi: 10.1038/nbt.1862 – volume: 3 start-page: 346 year: 2008 ident: 666_CR22 publication-title: Cell Stem Cell. doi: 10.1016/j.stem.2008.08.014 – volume: 21 start-page: 1107 year: 2014 ident: 666_CR32 publication-title: Cell Death Differ. doi: 10.1038/cdd.2014.28 – volume: 8 start-page: 376 year: 2011 ident: 666_CR9 publication-title: Cell Stem Cell. doi: 10.1016/j.stem.2011.03.001 – volume: 14 start-page: 1114 year: 2012 ident: 666_CR5 publication-title: Nat Cell Biol. doi: 10.1038/ncb2613 – volume: 4 start-page: 80 year: 2013 ident: 666_CR44 publication-title: Front Genet. doi: 10.3389/fgene.2013.00080 – volume: 12 start-page: 613 year: 2012 ident: 666_CR49 publication-title: Nat Rev Cancer. doi: 10.1038/nrc3318 – volume: 12 start-page: 253 year: 2011 ident: 666_CR4 publication-title: Nat Rev Genet. doi: 10.1038/nrg2955 – volume: 228 start-page: 9 year: 2013 ident: 666_CR27 publication-title: J Cell Physiol. doi: 10.1002/jcp.24104 – volume: 34 start-page: 232 year: 2010 ident: 666_CR17 publication-title: Comput Biol Chem. doi: 10.1016/j.compbiolchem.2010.08.001 – volume: 37 start-page: 3464 year: 2009 ident: 666_CR16 publication-title: Nucleic Acids Res. doi: 10.1093/nar/gkp205 – volume: 11 start-page: 197 year: 2009 ident: 666_CR51 publication-title: Nat Cell Biol. doi: 10.1038/ncb1827 – volume: 8 start-page: 166 year: 2007 ident: 666_CR18 publication-title: BMC Genomics. doi: 10.1186/1471-2164-8-166 – volume: 278 start-page: 37722 year: 2003 ident: 666_CR48 publication-title: J Biol Chem. doi: 10.1074/jbc.M301979200 – volume: 281 start-page: 23319 year: 2006 ident: 666_CR53 publication-title: J Biol Chem. doi: 10.1074/jbc.M601811200 – volume: 4 start-page: 3852 year: 2014 ident: 666_CR15 publication-title: Sci Rep. doi: 10.1038/srep03852 – volume: 12 start-page: 754 year: 2014 ident: 666_CR3 publication-title: Stem Cell Res. doi: 10.1016/j.scr.2014.03.007 – volume: 16 start-page: 62 year: 2014 ident: 666_CR19 publication-title: Neuro Oncol. doi: 10.1093/neuonc/not162 – volume: 7 start-page: 694 year: 2010 ident: 666_CR35 publication-title: Cell Stem Cell doi: 10.1016/j.stem.2010.11.010 – volume: 5 start-page: 12141 year: 2014 ident: 666_CR38 publication-title: Oncotarget. doi: 10.18632/oncotarget.2559 – volume: 46 start-page: 30 year: 2012 ident: 666_CR50 publication-title: Mol Cell. doi: 10.1016/j.molcel.2012.01.020 – volume: 4 start-page: 645 year: 2015 ident: 666_CR39 publication-title: Stem Cell Rep. doi: 10.1016/j.stemcr.2015.02.009 – volume: 15 start-page: 178 year: 2014 ident: 666_CR54 publication-title: Nat Rev Mol Cell Biol. doi: 10.1038/nrm3758 – volume: 110 start-page: 2858 year: 2013 ident: 666_CR12 publication-title: Proc Natl Acad Sci U S A. doi: 10.1073/pnas.1212769110 – volume: 19 start-page: 1525 year: 2012 ident: 666_CR43 publication-title: Cell Death Differ. doi: 10.1038/cdd.2012.30 – reference: 22622027 - Mol Cancer Res. 2012 Jul;10 (7):979-91 – reference: 21538421 - Prostate. 2012 Feb 1;72(2):117-28 – reference: 24311633 - Neuro Oncol. 2014 Jan;16(1):62-71 – reference: 28270145 - J Biomed Sci. 2017 Mar 7;24(1):20 – reference: 22767050 - J Mol Endocrinol. 2012 Jul 26;49(2):115-24 – reference: 21415849 - Nat Rev Genet. 2011 Apr;12(4):253-65 – reference: 24740298 - PLoS One. 2014 Apr 16;9(4):e95213 – reference: 16904174 - Cell. 2006 Aug 25;126(4):663-76 – reference: 24910449 - Semin Cell Dev Biol. 2014 Aug;32:98-106 – reference: 24551280 - Int J Clin Exp Pathol. 2014 Jan 15;7(2):602-10 – reference: 23386720 - Proc Natl Acad Sci U S A. 2013 Feb 19;110(8):2858-63 – reference: 25633840 - Cancer Lett. 2015 Apr 10;359(2):288-98 – reference: 21490602 - Nat Biotechnol. 2011 May;29(5):443-8 – reference: 25249788 - Int J Med Sci. 2014 Sep 13;11(11):1201-7 – reference: 23131918 - Nat Cell Biol. 2012 Nov;14(11):1114-21 – reference: 22020437 - Nat Cell Biol. 2011 Oct 23;13(11):1353-60 – reference: 16314309 - Nucleic Acids Res. 2005 Nov 27;33(20):e179 – reference: 21285944 - EMBO J. 2011 Mar 2;30(5):823-34 – reference: 22696098 - Stem Cells. 2012 Aug;30(8):1645-54 – reference: 24556840 - Nat Rev Mol Cell Biol. 2014 Mar;15(3):178-96 – reference: 24735951 - Stem Cell Res. 2014 May;12(3):754-61 – reference: 19136965 - Nat Cell Biol. 2009 Feb;11(2):197-203 – reference: 17554337 - Nature. 2007 Jun 28;447(7148):1130-4 – reference: 8474450 - Mol Cell Biol. 1993 May;13(5):2919-28 – reference: 21970405 - BMC Cancer. 2011 Oct 05;11:425 – reference: 16714766 - J Biol Chem. 2006 Aug 18;281(33):23319-25 – reference: 19896434 - Cell Stem Cell. 2009 Nov 6;5(5):457-8 – reference: 22258608 - Nature. 2012 Jan 18;481(7381):295-305 – reference: 21909390 - PLoS One. 2011;6(8):e24351 – reference: 22421968 - Cell Death Differ. 2012 Sep;19(9):1525-35 – reference: 22898542 - Nat Rev Cancer. 2012 Sep;12(9):613-26 – reference: 25801506 - Stem Cell Reports. 2015 Apr 14;4(4):645-57 – reference: 25303886 - Drugs R D. 2014 Dec;14 (4):253-64 – reference: 21474102 - Cell Stem Cell. 2011 Apr 8;8(4):376-88 – reference: 24458129 - Sci Rep. 2014 Jan 24;4:3852 – reference: 24608790 - Cell Death Differ. 2014 Jul;21(7):1107-18 – reference: 18786421 - Cell Stem Cell. 2008 Sep 11;3(3):346-353 – reference: 19339516 - Nucleic Acids Res. 2009 Jun;37(10):3464-73 – reference: 20128659 - Stem Cells Dev. 2010 Jul;19(7):935-50 – reference: 20863765 - Comput Biol Chem. 2010 Aug;34(4):232-41 – reference: 20870751 - Nucleic Acids Res. 2011 Feb;39(3):1054-65 – reference: 22552993 - J Cell Physiol. 2013 Jan;228(1):9-20 – reference: 25699255 - Front Cell Dev Biol. 2015 Feb 02;3:2 – reference: 17565689 - BMC Genomics. 2007 Jun 12;8:166 – reference: 25426550 - Oncotarget. 2014 Dec 15;5(23 ):12141-50 – reference: 21620789 - Cell Stem Cell. 2011 Jun 3;8(6):633-8 – reference: 23136034 - Stem Cells. 2013 Feb;31(2):259-68 – reference: 23681063 - Nat Rev Genet. 2013 Jun;14(6):427-39 – reference: 22387025 - Mol Cell. 2012 Apr 13;46(1):30-42 – reference: 12851404 - J Biol Chem. 2003 Sep 26;278(39):37722-9 – reference: 23831024 - Cell Rep. 2013 Jul 11;4(1):99-109 – reference: 20514025 - Oncogene. 2010 Aug 5;29(31):4378-87 – reference: 23717325 - Front Genet. 2013 May 13;4:80 – reference: 21112564 - Cell Stem Cell. 2010 Dec 3;7(6):694-707 |
| SSID | ssj0000330064 |
| Score | 2.2860827 |
| Snippet | Background
Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced pluripotent stem... Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to 'reprogram' somatic cells to become induced pluripotent stem cells... Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to 'reprogram' somatic cells to become induced pluripotent stem... A miR-524-5p precursor was introduced into human fibroblast HFF-1 in the presence of OSKM, and the relative number of embryonic stem cell (ESC)-like colonies... Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced pluripotent stem... Abstract Background Introduction of the transcription factors Oct4, Sox2, Klf4, and c-Myc (OSKM) is able to ‘reprogram’ somatic cells to become induced... |
| SourceID | doaj pubmedcentral proquest gale pubmed crossref springer |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 214 |
| SubjectTerms | Alkaline phosphatase Apoptosis Biomedical and Life Sciences Biomedical Engineering and Bioengineering c-Myc protein C19MC Cancer Carrier Proteins - genetics Carrier Proteins - metabolism Cell Biology Cell cycle Cell death Cell Line, Tumor Cell proliferation Cell regulation Cellular Reprogramming Chromosome 19 Colonies Epithelial-Mesenchymal Transition Fibroblasts Gene expression Gene targeting Genetic aspects Genomes Health aspects Heat-Shock Proteins - genetics Heat-Shock Proteins - metabolism Humans Inhibitory postsynaptic potentials Kinases KLF4 protein Life Sciences Mesenchyme MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miR-524-5p miRNA Myc protein Oct-4 protein Phylogeny Pluripotency Pluripotency genes Polymerase chain reaction Prostate Proteins Regenerative Medicine/Tissue Engineering Reprogramming efficiency Smad4 protein Smad4 Protein - genetics Smad4 Protein - metabolism Somatic cells Stem cell transplantation Stem Cells Transcription factors Zinc Finger E-box Binding Homeobox 2 - genetics Zinc Finger E-box Binding Homeobox 2 - metabolism |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3Ni9QwFA-yKHgRv62uGkUQlLBNmzbNcRx2cQ87DOsIewuZNFkHdtth2hG8-4f7Xtop0xX14pzK5BXS917eR_vLL4S8M4kwKhWCpWWioEGxCVv6FBGOXsSFLGJjfThsQs5mxcWFmu8d9YWYsI4euFPckbI81DAINBMc-XJ4yiHnQqbxcZmHfeRQ9ew1UyEGQ5sOybb_jMmL_KiBtqvAOSDaK89ZOkpEga__96i8l5ZuQiZvfDcN6ejkPrnX15F00s3_AbnlqofkTney5I9H5Of16hy6P8GyNa09hSqPrpFXonUM91YiPohOuTqbUhCcTai92iJjAu2A4Q1dzLP0dD7jjJqqpMdnC2Z6O7qSXmJ8pG1NN91B9o7i63_Es1LkyAyAr2uY9WPy9eR4Mf3M-gMXmJWpaJkH41gPBYTNuZVW2KwwpnQqV14V2VIaZQq4xJ4KOupcWiO9cA5MtMy49GX6hBxUdeWeEWp5bhNZWuFizJOZgc6Fi6TMbQm_jEck3mlf256NHA_FuNKhKyly3RlMg8E0GkynEfkw3LLuqDj-JvwJTToIIot2-AN8S_e-pf_lWxF5jQ6huy2pQyzQEyiiFURDWUTkbZBAJo0KoTqXZts0-vTL-UjofS_ka3hGa_qdD6ApJN8aSR6OJGGp2_HwzjN1H2oazRW-HBVKgk7fDMN4J8LnKldvg0yGtVqSRORp58iDZqDjhqZWwMPKkYuPVDceqVbfAhE51M7IeBeRj7vFsDetP1nm-f-wzAtyNwlLWbFEHZKDdrN1L8lt-71dNZtXIRb8AmaLWNg priority: 102 providerName: Directory of Open Access Journals – databaseName: ProQuest Central dbid: BENPR link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3db9MwELegA4kXvj8CAwxCQgJZixMnjp9QV3ViD6uqUqS9WZ6TlEpbUpoWiXf-cO4cNyxD7IU-RfVFin3n85398-8IeWciYVQsBIvzSEGCYiN2VsaIcCxFmMksNLZ0xSbkZJKdnqqp33BrPKxy5xOdo85ri3vkB5BsgykJJfmn1XeGVaPwdNWX0LhJ9pCpTAzI3uF4Mp11uywhpOuw6PrjTJ6lBw2kXxl-C6K-0pTFvQXJ8fb_7Z0vLU9XoZNXzk_dsnR07387dJ_c9QEpHbYW9IDcKKqH5HZbovLnI_LrYjmDNFKwZEXrkkK4SFdIULEpGF7SRKARHXF1MqIgOBlSe75F6gXaIswbOp8m8fF0whk1VU7HJ3NmvEEUOV2go6Wbmq6LBZYRKyieIyAwliLZpkOOXUC3H5OvR-P56DPzlRuYlbHYsBK0bEuIRGzKrbTCJpkxeaFSVaosOZNGmQweMTmD1DyV1shSFIWy_CzhsszjJ2RQ1VXxjFDLUxvJ3IoixAU3MZACcRHlqc3hl_CAhDv1aetpzbG6xrl26U2W6lbjGjSuUeM6DsiH7pVVy-lxnfAh2kQniHTc7o96vdB-dmv4cBdoIxpScCR14jGHwBDCoTLMUxmQ12hRur3b2jkVPYRoXIFblVlA3joJpOSoEPOzMNum0cdfZj2h916orKGP1vgrFDBSyOLVk9zvSYLPsP3mnU1q77Ma_ccgA_Kma8Y3EYdXFfXWySQY9EVRQJ62M6EbGUjdITsW0FnZmyO9oeu3VMtvjtEcgnCkzgvIx91suvRZ_9LM8-s78YLcidwsVyxS-2SwWW-Ll-SW_bFZNutX3lH8Bpgia4Q priority: 102 providerName: ProQuest |
| Title | miR-524-5p of the primate-specific C19MC miRNA cluster targets TP53IPN1- and EMT-associated genes to regulate cellular reprogramming |
| URI | https://link.springer.com/article/10.1186/s13287-017-0666-3 https://www.ncbi.nlm.nih.gov/pubmed/28962647 https://www.proquest.com/docview/1947934971 https://www.proquest.com/docview/1945224122 https://pubmed.ncbi.nlm.nih.gov/PMC5622517 https://doaj.org/article/9c1999161993419780131273381f0d67 |
| Volume | 8 |
| WOSCitedRecordID | wos000412195400018&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVADU databaseName: Open Access: BioMedCentral Open Access Titles customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: RBZ dateStart: 20100101 isFulltext: true titleUrlDefault: https://www.biomedcentral.com/search/ providerName: BioMedCentral – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: DOA dateStart: 20100101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVHPJ databaseName: ROAD: Directory of Open Access Scholarly Resources customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: M~E dateStart: 20100101 isFulltext: true titleUrlDefault: https://road.issn.org providerName: ISSN International Centre – providerCode: PRVPQU databaseName: Biological Science Database customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: M7P dateStart: 20150101 isFulltext: true titleUrlDefault: http://search.proquest.com/biologicalscijournals providerName: ProQuest – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: 7X7 dateStart: 20150101 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: BENPR dateStart: 20150101 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: Publicly Available Content Database customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: PIMPY dateStart: 20150101 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVAVX databaseName: SpringerLink Contemporary customDbUrl: eissn: 1757-6512 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000330064 issn: 1757-6512 databaseCode: RSV dateStart: 20100301 isFulltext: true titleUrlDefault: https://link.springer.com/search?facet-content-type=%22Journal%22 providerName: Springer Nature |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFLbYBhIv3C-BUQxCQgJF1IkT249d1Yk-tIq6gsaT5TpJqbQlVdMi8c4P5xwnjZZxkaAPVRUfV_GxfS7258-EvDEBNyrk3A_TQEGCYgN_kYeIcMx5XwrZNzZ3l02I6VSen6ukOcdd7dHu-y1JZ6ndtJbxhwryJol_gnCtOPbDA3IE3k7ibJydfW4XVvqQoYOfbXYwf1uz44McVf-vBvmKR7qOlry2Zeo80end_2rDPXKnCTzpoB4p98mNrHhAbtVXUX5_SH5crmaQLnI_WtMypxAW0jUSUWwzHw9jIqCIDpmaDCkITgfUXuyQYoHWSPKKzpMoHCdT5lNTpHQ0mfum6fgspUs0qHRb0k19831Gcb8AAbAUSTUdQuwS2vGIfDodzYcf_eaGBt-KkG_9HHrT5hBx2JhZYbmNpDFppmKVKxkthFFGwk9MwiAFj4U1IudZpixbREzkafiYHBZlkT0l1LLYBiK1POujY40MpDqMB2lsU_hEzCP9fZ9p29CX4y0aF9qlMTLWtXI1KFejcnXokXdtlXXN3fE34RMcCK0g0m67B-VmqZtZrOHFXUCNqEfOkLyJhQwCQAh78n4aC4-8xGGk6zOsrfHQA4i6FZhPIT3y2kkg9UaB2J6l2VWVHp_NOkJvG6G8hDZa0xyVAE0hW1dH8rgjCbbBdov341k3tqnSTOFqKlcCdPqqLcaaiLcrsnLnZCIM7oLAI0_q4d9qBlJ0yII5NFZ0JkZHdd2SYvXVMZdDsI0UeR55v58eV17rTz3z7J-kn5PbgZtfyg_UMTncbnbZC3LTftuuqk2PHIhz4b5ljxydjKbJrOeWYXoI-k3gWTKeJF96zqT8BJVHZqg |
| linkProvider | Springer Nature |
| linkToHtml | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1bb9MwFLbGAMEL90tgMINASKBodeLE8QNCpWxatbWaRif1zbiOUyptSWla0N75PfxGznHSsgyxtz3Qp6o5qWzn3L748zmEvNIB1zLk3A_TQAJAMYE_ykJkOGa8lYikpU3mmk2Ifj8ZDuXBGvm1PAuDtMqlT3SOOi0MviPfArANqsSlYB-m33zsGoW7q8sWGpVa7NnTHwDZyvfdT_B8XwfBzvags-vXXQV8I0I-9zMYgckgSpqYGWG4iRKtUytjmckkGgktdQJfETgAbIyF0SLj1krDRhETWRrC_14hV8GPC6SQiaFYvdNphSGG-HrzlCXxVglgL8GZI8csjv2wEf5cl4C_Y8GZYHieqHlut9YFwZ3b_9vy3SG36nSbtiv7uEvWbH6PXK8acJ7eJz9PJocAkrkfTWmRUUiG6RTLb8ytj0dQkUZFO0z2OhQE-21qjhdYWIJW_PmSDg6isHvQZz7VeUq3ewNf1-puUzrGMELnBZ3ZMTZJsxR3SZD2S7GUqOPFncAyPyBHl7IED8l6XuT2MaGGxSYQqeG2helEpAHgMR6ksUnhEzGPtJbqokxdtB17hxwrB96SWFUapkDDFGqYCj3ydnXLtKpYcpHwR9TBlSAWG3c_FLOxqn2XgoE7GIFcT86wZBULGaS9kOxlrTQWHtlEDVbVyd2Vy1RtwBoSgoZIPPLSSWDBkRwZTWO9KEvV_XzYEHpTC2UFzNHo-oAIrBTWKGtIbjQkwSOa5uWlDajaI5fqjwF45MXqMt6JLMPcFgsnE2FKGwQeeVRZ3mplgkQC9ucwWdGwycbSNa_kk6-uXjtADCwM6JF3S-s9M6x_PZknF09ik9zYHfT21X63v_eU3Aych5F-IDfI-ny2sM_INfN9Pilnz52LouTLZRv1b7JryBo |
| linkToPdf | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3rb9MwELdgPMQX3o_AYAYhIQ1Fy8OJ44-lrKKCVdVW0L5ZrmOXSltSNSkS3_nDuXPSaBkPCdFPVX2u4rPvfL_4_DtCXquIKREz5sd5JACg6Mif2xgzHC0LMp4FSltXbIJPJtnpqZi2dU6rbbb79kiyudOALE1FfbDKbWPiWXpQAYbK8A8xdStN_fgqucawZhDC9ZMv3UuWANA67LntaeZve_b2I0fb_6tzvrA7Xc6cvHR86nal0Z3_Hs9dcrsNSOmgWUH3yBVT3Cc3mhKV3x-QH-fLY4CRzE9WtLQUwkW6QoKK2vh4SRMTjegwFEdDCoKTAdVnG6ReoE2GeUVn0yQeTyehT1WR08Ojma_aBWFyukBHS-uSrs0Cy4gZiucImBhLkWzTZY6dw5geks-jw9nwg99WbvA1j1ntW5hlbSES0WmouWY6yZTKjUiFFVky50qoDL4iOANonnKtuGXGCB3Ok5DbPH5EdoqyME8I1WGqI55rZgLccBMFEChkUZ7qHD5J6JFgO39St7TmWF3jTDp4k6WyUa4E5UpUrow9st91WTWcHn8TfoeLohNEOm73Q7leyNa6JTy4C7QxG5KFSOoUxiEEhhAO2SBPuUf2cEnJ5m5r51TkAKJxAW6VZx555SSQkqPAnJ-F2lSVHJ8c94TetEK2hDFq1V6hAE0hi1dPcrcnCT5D95u3a1u2PquSocC3rExw0OnLrhl7Yh5eYcqNk0kw6IsijzxuTKHTDEB3QMcMBst7RtJTXb-lWH51jOYQhCN1nkfebk3lwmP9aWae_pP0Hrk5fT-Sn8aTj8_IrciZmvAjsUt26vXGPCfX9bd6Wa1fOA_yE9sha2s |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=miR-524-5p+of+the+primate-specific+C19MC+miRNA+cluster+targets+TP53IPN1-+and+EMT-associated+genes+to+regulate+cellular+reprogramming&rft.jtitle=Stem+cell+research+%26+therapy&rft.au=Huang%2C+Chiu-Jung&rft.au=Sugii%2C+Shigeki&rft.au=Kamarul%2C+Tunku&rft.au=Choo%2C+Kong+Bung&rft.date=2017-09-29&rft.pub=BioMed+Central+Ltd&rft.issn=1757-6512&rft.eissn=1757-6512&rft.volume=8&rft.issue=1&rft_id=info:doi/10.1186%2Fs13287-017-0666-3&rft.externalDBID=n%2Fa&rft.externalDocID=A507903178 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1757-6512&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1757-6512&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1757-6512&client=summon |