Suchergebnisse - "Endoplasmic Reticulum Stress/drug effects"

Osthole ameliorates wear particle-induced osteogenic impairment by mitigating endoplasmic reticulum stress via PERK signaling cascade

Autoren: Yu, Xin Jiang, Juan Li, Cheng et al.

Quelle: Mol Med
Molecular Medicine, Vol 30, Iss 1, Pp 1-26 (2024)

Schlagwörter: Male, 0301 basic medicine, Apoptosis, RM1-950, QD415-436, Osteolysis, Biochemistry, Mice, eIF-2 Kinase, 03 medical and health sciences, Coumarins, Osteogenesis, Animals, Humans, Aseptic loosening, 0303 health sciences, Osteoblasts, Osteoblast, Research, PERK signaling cascade, Osthole, Endoplasmic Reticulum Stress, Disease Models, Animal, Therapeutics. Pharmacology, Osteogenesis/drug effects [MeSH], eIF-2 Kinase/metabolism [MeSH], Endoplasmic Reticulum Stress/drug effects [MeSH], Osteoblasts/metabolism [MeSH], Coumarins/pharmacology [MeSH], Osteolysis/etiology [MeSH], Osteolysis/drug therapy [MeSH], Male [MeSH], Coumarins/chemistry [MeSH], Coumarins/therapeutic use [MeSH], Signal Transduction/drug effects [MeSH], Osteolysis/metabolism [MeSH], Disease Models, Animal [MeSH], Humans [MeSH], Apoptosis/drug effects [MeSH], Animals [MeSH], Evolutionary Aspects of Metabolic Diseases, ER stress, Mice [MeSH], Osteoblasts/drug effects [MeSH], Signal Transduction

Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/39707212
https://doaj.org/article/1db7541146d54e5b9afcf2a60182b294
https://repository.publisso.de/resource/frl:6517784

PPARβ/δ upregulates the insulin receptor β subunit in skeletal muscle by reducing lysosomal activity and EphB4 levels

Autoren: Wang, J.R. Jurado-Aguilar, J. Barroso, E. et al.

Quelle: Cell Commun Signal
Cell Communication and Signaling, Vol 22, Iss 1, Pp 1-12 (2024)
Cell communication and signaling, vol. 22, no. 1, pp. 595

Schlagwörter: Muscle Fibers, Skeletal, Cell Line, Mice, PPARβ/δ, Animals, PPAR delta, Muscle, Skeletal, PPAR-beta, Mice, Knockout, InsRβ, QH573-671, Research, Tunicamycin, EphB4, Endoplasmic Reticulum Stress, Receptor, Insulin, Up-Regulation, Mice, Inbred C57BL, Thiazoles, GW5101516, Medicine, ER stress, Cytology, Lysosomes, Lysosomes/metabolism, Receptor, Insulin/metabolism, Receptor, Insulin/genetics, Muscle, Skeletal/metabolism, Muscle, Skeletal/drug effects, PPAR-beta/metabolism, PPAR-beta/genetics, PPAR-beta/agonists, PPAR delta/metabolism, PPAR delta/genetics, Endoplasmic Reticulum Stress/drug effects, Up-Regulation/drug effects, Muscle Fibers, Skeletal/metabolism, Muscle Fibers, Skeletal/drug effects, Tunicamycin/pharmacology, Thiazoles/pharmacology

Dateibeschreibung: application/pdf

Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/39696437
https://doaj.org/article/f82685bf6b3848479236aa39cae3b0ba
https://serval.unil.ch/notice/serval:BIB_24B5A081A64A
https://serval.unil.ch/resource/serval:BIB_24B5A081A64A.P001/REF.pdf
http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_24B5A081A64A3

ER stress inhibition enhances formation of triacylglcerols and protects endothelial cells from lipotoxicity

Autoren: Kovačević, Igor Schmidt, Paula Henriette Kowalski, Annkatrin et al.

Quelle: Cell Commun Signal
Cell Communication and Signaling, Vol 22, Iss 1, Pp 1-21 (2024)

Schlagwörter: 0301 basic medicine, Palmitates, Ceramides, Cholesterol/metabolism, 03 medical and health sciences, Ceramides/metabolism, SDG 3 - Good Health and Well-being, Triglycerides/metabolism, Autophagy/drug effects, Endoplasmic Reticulum Stress/drug effects, Autophagy, Humans, Endothelial dysfunction, Obesity, Triglycerides, Endothelial Cells/drug effects, ddc:610, 0303 health sciences, QH573-671, Research, Endothelial Cells, Endoplasmic Reticulum Stress, Lipidomic analysis, Cholesterol, Medicine, Palmitates/pharmacology, ER stress, Cytology

Dateibeschreibung: application/pdf

Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/38831326
https://doaj.org/article/44ebdf5ee38d495d9485c5017c5c057d

Suppression of DYRK1A/B Drives Endoplasmic Reticulum Stress-mediated Autophagic Cell Death Through Metabolic Reprogramming in Colorectal Cancer Cells

Autoren: Jieon, Hwang Areum, Park Chinwoo, Kim et al.

Weitere Verfasser: Jieon, Hwang Areum, Park Chinwoo, Kim et al.

Quelle: Anticancer Research. 42:589-598

Schlagwörter: 0301 basic medicine, Apoptosis, Endoplasmic Reticulum, Colorectal Neoplasms / genetics, Mice, Protein Serine-Threonine Kinases / antagonists & inhibitors, Autophagic Cell Death / drug effects, Enzyme Inhibitors, 0303 health sciences, Tumor, Fluorouracil / pharmacology, Protein Serine-Threonine Kinases / genetics, Protein-Tyrosine Kinases / antagonists & inhibitors, Protein-Tyrosine Kinases, Cellular Reprogramming, Endoplasmic Reticulum Stress, Colorectal Neoplasms / drug therapy, 3. Good health, DYRK1A protein, endoplasmic reticulum stress, Fluorouracil, Colorectal Neoplasms, Glycolysis, Metabolic Networks and Pathways, autophagy, Autophagic Cell Death, colorectal cancer, Protein Serine-Threonine Kinases, Apoptosis / drug effects, Cellular Reprogramming / genetics, Colorectal Neoplasms / pathology, Cell Line, 03 medical and health sciences, Cell Line, Tumor, Autophagy / drug effects, Autophagy, Endoplasmic Reticulum / drug effects, Animals, Humans, Metabolic Networks and Pathways / drug effects, Glycolysis / drug effects, Cell Proliferation, Enzyme Inhibitors / pharmacology, protein kinases, Endoplasmic Reticulum Stress / drug effects, Protein-Tyrosine Kinases / genetics, Reactive Oxygen Species / metabolism, Endoplasmic Reticulum / genetics, Xenograft Model Antitumor Assays, DYRK1B protein, Cell Proliferation / drug effects, Reactive Oxygen Species

Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/34969768

Endoplasmic Reticulum Stress Mediates Vascular Smooth Muscle Cell Calcification via Increased Release of Grp78 (Glucose-Regulated Protein, 78 kDa)-Loaded Extracellular Vesicles

Autoren: Malgorzata Furmanik Jayanta Bordoloi Meredith Whitehead et al.

Quelle: Arterioscler Thromb Vasc Biol

Schlagwörter: TRANSCRIPTION FACTOR 4, Male, 0301 basic medicine, ARTERIAL CALCIFICATION, Extracellular Vesicles/drug effects, Muscle, Smooth, Vascular, ACTIVATION, arteries, Rats, Sprague-Dawley, 0302 clinical medicine, Translational Sciences, Heat-Shock Proteins/genetics, Endoplasmic Reticulum Chaperone BiP, Vascular/drug effects, Smooth Muscle/metabolism, Cells, Cultured, Heat-Shock Proteins, 0303 health sciences, Cultured, Middle Aged, Endoplasmic Reticulum Stress, Warfarin/toxicity, APOPTOSIS, Vascular Calcification/chemically induced, eIF-2 Kinase/genetics, endoplasmic reticulum, vascular calcification, Muscle, Female, Smooth, Signal Transduction, Activating Transcription Factor 4/genetics, Adult, Adolescent, Cells, Myocytes, Smooth Muscle, INHIBITION, MATRIX GLA-PROTEIN, CALCIUM, OSTEOBLAST DIFFERENTIATION, MECHANISMS, Young Adult, Extracellular Vesicles, 03 medical and health sciences, Endoplasmic Reticulum Stress/drug effects, KINASE, Animals, Humans, Aged, Myocytes, Animal, aging, Activating Transcription Factor 4, Rats, warfarin, Disease Models, Animal, Gene Expression Regulation, Disease Models, Sprague-Dawley

Zugangs-URL: https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.120.315506
https://pubmed.ncbi.nlm.nih.gov/33297752
https://europepmc.org/article/PMC/PMC7837691
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7837691
https://www.ahajournals.org/doi/10.1161/ATVBAHA.120.315506
https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.120.315506
https://pubmed.ncbi.nlm.nih.gov/33297752/

Autophagy alleviates amiodarone-induced hepatotoxicity

Autoren: Franziska Wandrer Živa Frangež Stephanie Liebig et al.

Quelle: Arch Toxicol
Wandrer, Franziska; Frangež, Živa; Liebig, Stephanie; John, Katharina; Vondran, Florian; Wedemeyer, Heiner; Veltmann, Christian; Pfeffer, Tobias J; Shibolet, Oren; Schulze-Osthoff, Klaus; Simon, Hans-Uwe; Bantel, Heike (2020). Autophagy alleviates amiodarone-induced hepatotoxicity. Archives of toxicology, 94(10), pp. 3527-3539. Springer-Verlag 10.1007/s00204-020-02837-9 <http://dx.doi.org/10.1007/s00204-020-02837-9>

Schlagwörter: Male, 0301 basic medicine, Aged [MeSH], Cell Survival [MeSH], Endoplasmic Reticulum Stress/drug effects [MeSH], Keratin-18, Keratin-18/blood [MeSH], Chloroquine/pharmacology [MeSH], Gene Knockout Techniques [MeSH], Drug-induced liver injury, Anti-Arrhythmia Agents/adverse effects [MeSH], Male [MeSH], CRISPR-Cas Systems [MeSH], Autophagy [MeSH], Amiodarone, Hepatocytes/drug effects [MeSH], Female [MeSH], Autophagy, Humans [MeSH], Apoptosis/drug effects [MeSH], Apoptosis, Organ Toxicity and Mechanisms, Hep G2 Cells [MeSH], Lipid Metabolism/drug effects [MeSH], ER stress, Chemical and Drug Induced Liver Injury [MeSH], Amiodarone/adverse effects [MeSH], Cells, Cultured [MeSH], Cell Survival, 610 Medicine & health, Chloroquine, Hep G2 Cells, Endoplasmic Reticulum Stress, Lipid Metabolism, 3. Good health, Gene Knockout Techniques, 03 medical and health sciences, Hepatocytes, Humans, Female, CRISPR-Cas Systems, Chemical and Drug Induced Liver Injury, Anti-Arrhythmia Agents, Cells, Cultured, Aged

Dateibeschreibung: application/pdf

Zugangs-URL: https://link.springer.com/content/pdf/10.1007/s00204-020-02837-9.pdf
https://pubmed.ncbi.nlm.nih.gov/32651653
https://europepmc.org/article/PMC/PMC7502042
https://pubmed.ncbi.nlm.nih.gov/32651653/
https://link.springer.com/article/10.1007/s00204-020-02837-9
https://www.ncbi.nlm.nih.gov/pubmed/32651653
http://www.ncbi.nlm.nih.gov/pubmed/32651653
https://link.springer.com/content/pdf/10.1007/s00204-020-02837-9.pdf
https://boris.unibe.ch/146612/
https://repository.publisso.de/resource/frl:6466338

Chronic activation of GPR40 does not negatively impact upon BRIN-BD11 pancreatic β-cell physiology and function

Autoren: Gabriela Nunes Marsiglio-Librais Noémie Karabacz Eloisa Aparecida Vilas-Boas et al.

Quelle: Pharmacol Rep

Schlagwörter: 0301 basic medicine, ddc:500, Cell Survival, Palmitates, β-cells, Apoptosis, GPR40 activation, Receptors, G-Protein-Coupled/metabolism [MeSH], Endoplasmic Reticulum Stress/drug effects [MeSH], Cell Line [MeSH], Palmitate, Receptors, G-Protein-Coupled/drug effects [MeSH], Propionates/pharmacology [MeSH], Benzoates/administration, Insulin-Secreting Cells/metabolism [MeSH], Propionates/administration, Pyrimidines/pharmacology [MeSH], Benzoates/pharmacology [MeSH], Calcium/metabolism [MeSH], Hydrogen Peroxide/metabolism [MeSH], Palmitates/toxicity [MeSH], Apoptosis/drug effects [MeSH], Rats [MeSH], Cell Survival/drug effects [MeSH], Pyrimidines/administration, Animals [MeSH], Article, Methylamines/pharmacology [MeSH], Lipotoxicity, Methylamines/administration, Cell Proliferation/drug effects [MeSH], Benzoates, Cell Line, Receptors, G-Protein-Coupled, Methylamines, 03 medical and health sciences, Insulin-Secreting Cells, Animals, Cell Proliferation, 2. Zero hunger, ddc:610, 0303 health sciences, Hydrogen Peroxide, Endoplasmic Reticulum Stress, Rats, 3. Good health, Pyrimidines, Calcium, Propionates

Zugangs-URL: https://link.springer.com/content/pdf/10.1007/s43440-020-00101-6.pdf
https://pubmed.ncbi.nlm.nih.gov/32274767
https://link.springer.com/content/pdf/10.1007/s43440-020-00101-6.pdf
https://pubmed.ncbi.nlm.nih.gov/32274767/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7704488
https://link.springer.com/article/10.1007/s43440-020-00101-6
https://repository.publisso.de/resource/frl:6472212

Inhibition of oxygen-sensing prolyl hydroxylases increases lipid accumulation in human primary tubular epithelial cells without inducing ER stress

Autoren: Gunnar Schley Steffen Grampp Margarete Goppelt-Struebe

Quelle: Cell Tissue Res

Schlagwörter: Male, 0301 basic medicine, 0303 health sciences, Regular Article, Epithelial Cells, Mice, Transgenic, Prolyl-Hydroxylase Inhibitors, Endoplasmic Reticulum Stress, Lipid Metabolism, Hypoxia-Inducible Factor-Proline Dioxygenases, 3. Good health, Mice, Inbred C57BL, Mice, 03 medical and health sciences, Prolyl hydroxylase inhibitors, Mice, Inbred C57BL [MeSH], Endoplasmic Reticulum Stress/drug effects [MeSH], Kidney Tubules/cytology [MeSH], Humans [MeSH], Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists, Prolyl-Hydroxylase Inhibitors/therapeutic use [MeSH], Animals [MeSH], Lipid Metabolism/drug effects [MeSH], Epithelial Cells/drug effects [MeSH], Kidney Diseases/drug therapy [MeSH], Mice, Transgenic [MeSH], ER stress, Mice [MeSH], Cyclosporine A, Human primary tubular epithelial cells, Male [MeSH], Prolyl-Hydroxylase Inhibitors/pharmacology [MeSH], Cells, Cultured [MeSH], Lipid accumulation, Kidney Tubules/drug effects [MeSH], Kidney Tubules, Animals, Humans, Kidney Diseases, ddc:610, Cells, Cultured

Dateibeschreibung: application/pdf

Zugangs-URL: https://link.springer.com/content/pdf/10.1007/s00441-020-03186-w.pdf
https://pubmed.ncbi.nlm.nih.gov/32189058
https://link.springer.com/content/pdf/10.1007/s00441-020-03186-w.pdf
https://paperity.org/p/233806493/inhibition-of-oxygen-sensing-prolyl-hydroxylases-increases-lipid-accumulation-in-human
https://pubmed.ncbi.nlm.nih.gov/32189058/
https://pubag.nal.usda.gov/catalog/6998235
https://www.scilit.net/article/0fbab79c622c04e0b89b5a35dd4d2698
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7306052
https://opus4.kobv.de/opus4-fau/files/22924/s00441-020-03186-w.pdf
https://repository.publisso.de/resource/frl:6469444

Distinct effects of inflammation on gliosis, osmohomeostasis, and vascular integrity during amyloid beta-induced retinal degeneration.

Autoren: Dinet, V. Bruban, J. Chalour, N. et al.

Schlagwörter: Amyloid beta-Peptides/administration & dosage, Amyloid beta-Peptides/toxicity, Animals, Apoptosis/drug effects, Blood-Retinal Barrier/drug effects, Blood-Retinal Barrier/pathology, Endoplasmic Reticulum Stress/drug effects, Gene Expression/drug effects, Gliosis/pathology, Homeostasis/drug effects, Inflammation/pathology, Mice, Inbred C57BL, Peptide Fragments/administration & dosage, Peptide Fragments/toxicity, Photoreceptor Cells, Vertebrate/drug effects, Vertebrate/pathology, Retina/drug effects, Retina/pathology, Retinal Degeneration/genetics, Retinal Degeneration/pathology

Relation: Aging Cell; https://iris.unil.ch/handle/iris/217581; serval:BIB_CA62E3A6E44A; 000306400600015

Verfügbarkeit: https://iris.unil.ch/handle/iris/217581
https://doi.org/10.1111/j.1474-9726.2012.00834.x

Dysfunctional autophagy following exposure to pro-inflammatory cytokines contributes to pancreatic β-cell apoptosis.

Autoren: Lambelet, M. Terra, L.F. Fukaya, M. et al.

Schlagwörter: Animals, Apoptosis, Autophagosomes/drug effects, Autophagosomes/metabolism, Autophagosomes/ultrastructure, Autophagy, Cathepsin B/metabolism, Cell Line, Cell Survival/drug effects, Cytokines/toxicity, Endoplasmic Reticulum Stress/drug effects, Humans, Inflammation Mediators/toxicity, Insulin-Secreting Cells/drug effects, Insulin-Secreting Cells/metabolism, Insulin-Secreting Cells/pathology, Lysosomes/drug effects, Lysosomes/metabolism, Male, Mechanistic Target of Rapamycin Complex 1/metabolism, Mitochondrial Degradation/drug effects, Models, Biological, Multivesicular Bodies/drug effects, Multivesicular Bodies/metabolism, Multivesicular Bodies/ultrastructure, Rats, Wistar, Signal Transduction/drug effects, Time Factors

Dateibeschreibung: application/pdf

Relation: Cell Death & Disease; https://iris.unil.ch/handle/iris/167309; serval:BIB_CE4715907BDD; 000427384900013

Verfügbarkeit: https://iris.unil.ch/handle/iris/167309
https://doi.org/10.1038/s41419-017-0121-5

ATF4 leads to glaucoma by promoting protein synthesis and ER client protein load

Autoren: Kasetti, Ramesh B. Patel, Pinkal D. Maddineni, Prabhavathi et al.

Quelle: Nature Communications

Schlagwörter: Activating Transcription Factor 4 / antagonists & inhibitors, Activating Transcription Factor 4 /genetics, Activating Transcription Factor 4 /metabolism, Animals, Aqueous Humor / metabolism, Cell Death, Cells, Cultured, Endoplasmic Reticulum Stress / drug effects, Endoplasmic Reticulum Stress / genetics, Glaucoma, Open-Angle / drug therapy, Open-Angle / metabolism, Open-Angle / pathology, Humans, Mice, Ocular Hypertension / drug therapy, Ocular Hypertension / metabolism, Ocular Hypertension / pathology, Optic Nerve / metabolism, Optic Nerve / pathology, Protein Biosynthesis / drug effects, Protein Phosphatase 1 / genetics, Protein Phosphatase 1 / metabolism, Retinal Ganglion Cells / metabolism, Retinal Ganglion Cells / pathology, Signal Transduction, Trabecular Meshwork / drug effects, Trabecular Meshwork / metabolism, Trabecular Meshwork / pathology

Dateibeschreibung: application/pdf

Relation: https://doi.org/10.1038/s41467-020-19352-1; https://hdl.handle.net/20.500.12503/31990; 11

Verfügbarkeit: https://hdl.handle.net/20.500.12503/31990

Silica nanoparticle-induced oxidative stress and mitochondrial damage is followed by activation of intrinsic apoptosis pathway in glioblastoma cells

Autoren: Magdalena Kusaczuk Rafał Krętowski Monika Naumowicz et al.

Quelle: Int J Nanomedicine
International Journal of Nanomedicine, Vol Volume 13, Pp 2279-2294 (2018)

Schlagwörter: 0301 basic medicine, Medicine (General), mitochondrial damage, Mitochondria - metabolism, Glioblastoma - drug therapy, Brain neoplasms - drug therapy, Antineoplastic agents - pharmacology, Apoptosis, silica nanoparticles, International Journal of Nanomedicine, Endoplasmic Reticulum Chaperone BiP, Original Research, Gene expression regulation, 0303 health sciences, Brain Neoplasms, apoptosis, Endoplasmic Reticulum Stress, Silicon Dioxide, Silicon dioxide - pharmacology, Caspase 9, Mitochondria, 3. Good health, Gene Expression Regulation, Neoplastic, Glioblastoma - pathology, Endoplasmic reticulum stress - drug effects, ER stress, tumor, Apoptosis - drug effects, Antineoplastic Agents, Mitochondria - drug effects, Nanoparticles - administration & dosage, Brain neoplasms - pathology, 03 medical and health sciences, R5-920, Cell Line, Tumor, Animals, Humans, Silicon dioxide - administration & dosage, Transcription factor CHOP - metabolism, Endoplasmic reticulum stress - genetics, neoplastic, Antineoplastic agents - administration & dosage, Oxidative stress - drug effects, Nanoparticles - chemistry, Oxidative Stress, nanotoxicity, Nanoparticles, Brain neoplasms - metabolism, Cell line, Glioblastoma - metabolism, Glioblastoma, Transcription Factor CHOP

Dateibeschreibung: text/html

Zugangs-URL: https://www.dovepress.com/getfile.php?fileID=41501
https://pubmed.ncbi.nlm.nih.gov/29695906
https://doaj.org/article/a0100ab4c3e04149953f5d09ddee99b6
https://www.dovepress.com/silica-nanoparticle-induced-oxidative-stress-and-mitochondrial-damage--peer-reviewed-article-IJN
https://www.dovepress.com/silica-nanoparticle-induced-oxidative-stress-and-mitochondrial-damage--peer-reviewed-fulltext-article-IJN
https://www.dovepress.com/getfile.php?fileID=41501
https://doi.org/10.2147/IJN.S158393
https://europepmc.org/article/MED/29695906
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5905826
https://paperity.org/p/107567171/silica-nanoparticle-induced-oxidative-stress-and-mitochondrial-damage-is-followed-by
https://www.dovepress.com/silica-nanoparticle-induced-oxidative-stress-and-mitochondrial-damage--peer-reviewed-fulltext-article-IJN
https://doi.org/10.2147/IJN.S158393

ER-stress mobilization of death-associated protein kinase-1–dependent xenophagy counteracts mitochondria stress–induced epithelial barrier dysfunction

Autoren: Lopes, Fernando Keita, Åsa V Saxena, Alpana et al.

Quelle: Journal of Biological Chemistry, vol 293, iss 9

Schlagwörter: Male, 0301 basic medicine, Biomedical and clinical sciences, Crohn's Disease, Epithelium/drug effects, Medical and Health Sciences, Oral and gastrointestinal, intestinal barrier function, Epithelium, Oxidative Phosphorylation, Mice, oxidative metabolism, DAPK1, bacteria, Oxidative Phosphorylation/drug effects, Tumor, Escherichia coli/drug effects, Tunicamycin, Biological Sciences, Endoplasmic Reticulum Stress, Death-Associated Protein Kinases/metabolism, Mitochondria/drug effects, Mitochondria, 3. Good health, mitochondria, Biological sciences, endoplasmic reticulum stress, Female, epithelial barrier, autophagy, Biochemistry & Molecular Biology, Tunicamycin/pharmacology, Autoimmune Disease, Permeability, Cell Line, 03 medical and health sciences, inflammatory bowel disease, Cell Line, Tumor, Endoplasmic Reticulum Stress/drug effects, Escherichia coli, Animals, Humans, bacterial translocation, Aged, mitochondrial stress, Biomedical and Clinical Sciences, epithelial cell, Inflammatory Bowel Disease, Activating Transcription Factor 6/metabolism, Activating Transcription Factor 6, Death-Associated Protein Kinases, Chemical sciences, IBD basic research, Chemical Sciences, Biochemistry and Cell Biology, Digestive Diseases

Zugangs-URL: http://www.jbc.org/content/293/9/3073.full.pdf
https://pubmed.ncbi.nlm.nih.gov/29317503
http://liu.diva-portal.org/smash/record.jsf?pid=diva2%3A1199527
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5836131
https://www.jbc.org/article/S0021-9258(20)39046-3/fulltext
https://www.jbc.org/content/293/9/3073.full
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5836131
https://pubmed.ncbi.nlm.nih.gov/29317503/
https://escholarship.org/uc/item/1p21f9f6

Omics-based identification of the combined effects of idiosyncratic drugs and inflammatory cytokines on the development of drug-induced liver injury

Autoren: J. Jiang K. Mathijs L. Timmermans et al.

Weitere Verfasser: J. Jiang K. Mathijs L. Timmermans et al.

Quelle: Toxicology and Applied Pharmacology. 332:100-108

Schlagwörter: 0301 basic medicine, Drug-induced liver injury, MAP Kinase Signaling System, PROTEIN-KINASES, Liver/cytology, JNK ACTIVATION, Apoptosis, Signal transduction, Microarray, Ceramides, Ceramide, 03 medical and health sciences, Ceramides/metabolism, PROTEOMICS INVESTIGATIONS, Tandem Mass Spectrometry, tandem mass spectrometry, Endoplasmic Reticulum Stress/drug effects, Humans, Metabolomics, 0303 health sciences, Dose-Response Relationship, Drug, CERAMIDE, Gene Expression Profiling, Apoptosis/drug effects, NF-kappa B/genetics, Cytokines/metabolism, NF-kappa B, NECROSIS-FACTOR-ALPHA, Hep G2 Cells, HEPG2 CELLS, Toxicogenomics, Endoplasmic Reticulum Stress, APOPTOSIS, 3. Good health, Chemical and Drug Induced Liver Injury/metabolism, HUMAN HEPATOCYTES, Liver, Hepatocytes, Cytokines, Chemical and Drug Induced Liver Injury, Hepatocytes/drug effects, ER stress, INDUCED HEPATOTOXICITY, INDUCED CELL-DEATH, Signal Transduction

Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/28733206
https://cris.maastrichtuniversity.nl/en/publications/68f2bdfe-2846-4416-ad86-3f93cee315bf
https://doi.org/10.1016/j.taap.2017.07.014
https://www.sciencedirect.com/science/article/pii/S0041008X17303113
https://pubmed.ncbi.nlm.nih.gov/28733206/
https://cris.maastrichtuniversity.nl/portal/en/publications/omicsbased-identification-of-the-combined-effects-of-idiosyncratic-drugs-and-inflammatory-cytokines-on-the-development-of-druginduced-liver-injury(68f2bdfe-2846-4416-ad86-3f93cee315bf).html
https://www.narcis.nl/publication/RecordID/oai%3Acris.maastrichtuniversity.nl%3Apublications%2F68f2bdfe-2846-4416-ad86-3f93cee315bf
https://www.ncbi.nlm.nih.gov/pubmed/28733206
https://core.ac.uk/display/153359546
https://hdl.handle.net/20.500.14017/75cbb161-eeff-4b66-80a8-b86c8cf56dec
https://doi.org/10.1016/j.taap.2017.07.014
https://biblio.vub.ac.be/vubir/omicsbased-identification-of-the-combined-effects-of-idiosyncratic-drugs-and-inflammatory-cytokines-on-the-development-of-druginduced-liver-injury(75cbb161-eeff-4b66-80a8-b86c8cf56dec).html
https://biblio.vub.ac.be/vubir/omicsbased-identification-of-the-combined-effects-of-idiosyncratic-drugs-and-inflammatory-cytokines-on-the-development-of-druginduced-liver-injury(f437d2b6-d57a-4a87-a697-efec07a090ea).html
https://doi.org/10.1016/j.taap.2017.07.014

Combination of tauroursodeoxycholic acid and N‐acetylcysteine exceeds standard treatment for acetaminophen intoxication

Autoren: Annelies Paridaens Sarah Raevens Isabelle Colle et al.

Weitere Verfasser: Annelies Paridaens Sarah Raevens Isabelle Colle et al.

Quelle: Liver International. 37:748-756

Schlagwörter: Male, 0301 basic medicine, mice, Acetaminophen/poisoning, Taurochenodeoxycholic Acid/pharmacology, Oxidative Stress/drug effects, Apoptosis, Acetylcysteine/pharmacology, Taurochenodeoxycholic Acid, Mice, 03 medical and health sciences, Endoplasmic Reticulum Stress/drug effects, Unfolded Protein Response/drug effects, Animals, Alanine Transaminase/blood, Chemical and Drug Induced Liver Injury/drug therapy, Acetaminophen, 0303 health sciences, Apoptosis/drug effects, Cytokines/metabolism, Hepatocytes/metabolism, Alanine Transaminase, Endoplasmic Reticulum Stress, Acetylcysteine, 3. Good health, Mice, Inbred C57BL, Oxidative Stress, Liver, Hepatocytes, Unfolded Protein Response, Cytokines, Liver/pathology, Chemical and Drug Induced Liver Injury

Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/27706903
https://biblio.ugent.be/publication/8174562
https://pubmed.ncbi.nlm.nih.gov/27706903/
http://europepmc.org/abstract/MED/27706903
https://onlinelibrary.wiley.com/doi/10.1111/liv.13261
http://onlinelibrary.wiley.com/doi/10.1111/liv.13261/abstract
https://researchportal.vub.be/en/publications/combination-of-tauroursodeoxycholic-acid-and-n-acetylcysteine-exc

4-Phenylbutyric acid reduces mutant-TGFBIp levels and ER stress through activation of ERAD pathway in corneal fibroblasts of granular corneal dystrophy type 2

Autoren: Tae Im Kim Begum Akuzum Yong Sun Maeng et al.

Weitere Verfasser: Tae Im Kim Begum Akuzum Yong Sun Maeng et al.

Quelle: Biochemical and Biophysical Research Communications. 477:841-846

Schlagwörter: 0301 basic medicine, Hereditary/physiopathology, Down-Regulation/drug effects, Apoptosis, UPR, 4-Phenylbutyric acid, Cornea, Transforming Growth Factor beta, Cells, Cultured, Fibroblasts/metabolism, GCD2, Corneal Dystrophies, Hereditary, Extracellular Matrix Proteins, 0303 health sciences, Cultured, Endoplasmic Reticulum-Associated Degradation, Endoplasmic Reticulum Stress, Phenylbutyrates, 3. Good health, Extracellular Matrix Proteins/metabolism, Cornea/drug effects, Drug, Cornea/metabolism, ER stress, Corneal Dystrophies, Mutation/genetics, Phenylbutyrates/administration & dosage, Transforming Growth Factor beta/genetics, Cells, Cornea/physiopathology, TGFBIp, Down-Regulation, Transforming Growth Factor beta/metabolism, Extracellular Matrix Proteins/genetics, Dose-Response Relationship, Mutation/drug effects, 03 medical and health sciences, Hereditary/drug therapy, Humans, Hereditary/pathology, Dose-Response Relationship, Drug, Apoptosis/drug effects, ERAD, Fibroblasts, Endoplasmic Reticulum-Associated Degradation/drug effects, Fibroblasts/pathology, Fibroblasts/drug effects, Corneal fibroblasts, Mutation, Endoplasmic Reticulum Stress/drug effects

Zugangs-URL: https://pubmed.ncbi.nlm.nih.gov/27373828
http://www.ncbi.nlm.nih.gov/pubmed/27373828
https://ir.ymlib.yonsei.ac.kr/handle/22282913/151868
https://yonsei.pure.elsevier.com/en/publications/4-phenylbutyric-acid-reduces-mutant-tgfbip-levels-and-er-stress-t
https://www.sciencedirect.com/science/article/pii/S0006291X16310737
https://pubmed.ncbi.nlm.nih.gov/27373828/
https://europepmc.org/article/MED/27373828

Placental endoplasmic reticulum stress in gestational diabetes: the potential for therapeutic intervention with chemical chaperones and antioxidants: the potential for therapeutic intervention with chemical chaperones and antioxidants

Autoren: Yung, Hong-Wa Alnæs-Katjavivi, Patji Jones, Carolyn JP et al.

Weitere Verfasser: Yung, Hong-Wa Alnæs-Katjavivi, Patji Jones, Carolyn JP et al.

Quelle: Diabetologia
Yung, H-W, Alnæs-Katjavivi, P, Jones, C J P, El-Bacha, T, Golic, M, Staff, A-C & Burton, G J 2016, 'Placental endoplasmic reticulum stress in gestational diabetes : the potential for therapeutic intervention with chemical chaperones and antioxidants', Diabetologia, vol. 59, no. 10, pp. 2240-50. https://doi.org/10.1007/s00125-016-4040-2

Schlagwörter: Blood Glucose, 0301 basic medicine, Taurochenodeoxycholic Acid/pharmacology, Endocrinology, Diabetes and Metabolism, Placenta, Eukaryotic Initiation Factor-2, Phenylbutyrates/pharmacology, Ascorbic Acid, Antioxidants, Unfolded protein response, Pregnancy, Chaperones, Vitamin E, Phosphorylation, Gestational diabetes, Ascorbic Acid/pharmacology, 0303 health sciences, Blotting, Metabolic acidosis, Diabetes, Trophoblast, Phosphorylation/drug effects, Endoplasmic Reticulum Stress, Glucose/pharmacology, Phenylbutyrates, 3. Good health, Endoplasmic reticulum stress, Female, Acidosis, Western, Adult, Blotting, Western, Antioxidants/therapeutic use, Eukaryotic Initiation Factor-2/metabolism, Article, Cell Line, Taurochenodeoxycholic Acid, 03 medical and health sciences, Blood Glucose/drug effects, Endoplasmic Reticulum Stress/drug effects, Placenta/metabolism, Unfolded Protein Response/drug effects, Internal Medicine, Humans, Vitamin E/pharmacology, Diabetes, Gestational, Glucose, Acidosis/drug therapy, Cardiovascular and Metabolic Diseases, Unfolded Protein Response, Diabetes, Gestational/blood, Gestational/blood

Dateibeschreibung: application/pdf

Zugangs-URL: https://link.springer.com/content/pdf/10.1007/s00125-016-4040-2.pdf
https://pubmed.ncbi.nlm.nih.gov/27406815
https://research.manchester.ac.uk/en/publications/c8ce5083-9ae4-4885-ac79-64cfe3364d67
https://doi.org/10.1007/s00125-016-4040-2
https://link.springer.com/article/10.1007/s00125-016-4040-2
https://www.repository.cam.ac.uk/handle/1810/256684
https://europepmc.org/article/MED/27406815
https://pubmed.ncbi.nlm.nih.gov/27406815/
https://core.ac.uk/display/42340664
https://link.springer.com/article/10.1007/s00125-016-4040-2/fulltext.html
http://edoc.mdc-berlin.de/15852/1/15852oa.pdf

Sorcin Links Pancreatic β-Cell Lipotoxicity to ER Ca2+ Stores

Autoren: Marmugi Alice Parnis et al.

Weitere Verfasser: Marmugi Alice Parnis et al.

Quelle: Diabetes, Vol. 65, No 4 (2016) pp. 1009-21
DIABETES

Schlagwörter: 0301 basic medicine, Calcium-Binding Proteins/genetics/physiology, Mice, Obese, Endoplasmic Reticulum/drug effects/metabolism, Endoplasmic Reticulum, Obese, Mice, Obesity/metabolism/pathology, ENDOPLASMIC-RETICULUM STRESS, Insulin-Secreting Cells, IN-VIVO, 11 Medical and Health Sciences, Cells, Cultured, Mice, Knockout, 2. Zero hunger, 0303 health sciences, Cultured, ddc:617, Research Support, Non-U.S. Gov't, Insulin-Secreting Cells/drug effects/metabolism/pathology, ACTIVATED PROTEIN-KINASE, Endoplasmic Reticulum Stress, 3. Good health, RYANODINE RECEPTORS, OBESITY, ISLETS, Calcium Signaling/drug effects, Endoplasmic reticulum stress, HEART, CALCIUM-RELEASE, Life Sciences & Biomedicine, mice, Calcium/metabolism, Cells, Knockout, High-Fat/adverse effects, calcium signaling, Diet, High-Fat, Endocrinology & Metabolism, RESISTANT CELLS, 03 medical and health sciences, Dietary Fats/toxicity, Research Support, N.I.H., Extramural, STIMULATED INSULIN-SECRETION, Journal Article, Endoplasmic Reticulum Stress/drug effects, Animals, Calcium Signaling, Obesity, Science & Technology, Calcium-Binding Proteins, Dietary Fats, Diet, High-Fat, GLUCOSE-6-PHOSPHATASE, Calcium

Dateibeschreibung: application/pdf

Zugangs-URL: https://diabetes.diabetesjournals.org/content/diabetes/65/4/1009.full.pdf
https://pubmed.ncbi.nlm.nih.gov/26822088
https://moh-it.pure.elsevier.com/en/publications/sorcin-links-pancreatic-%CE%B2-cell-lipotoxicity-to-er-casup2sup-store
http://diabetes.diabetesjournals.org/content/early/2016/01/14/db15-1334
https://www.ncbi.nlm.nih.gov/pubmed/26822088
https://diabetes.diabetesjournals.org/content/diabetes/65/4/1009.full.pdf
https://serval.unil.ch/notice/serval:BIB_FD358A981FEB
https://core.ac.uk/display/80266286
http://hdl.handle.net/10044/1/29397
https://archive-ouverte.unige.ch/unige:100303
https://archive-ouverte.unige.ch/unige:100303
https://doi.org/10.2337/db15-1334
http://diabetes.diabetesjournals.org/content/65/4/1009
https://doi.org/10.2337/db15-1334
https://hdl.handle.net/11568/778795

Inhibition of endoplasmic reticulum chaperone protein glucose-regulated protein 78 potentiates anti-angiogenic therapy in renal cell carcinoma through inactivation of the PERK/eIF2α pathway

Autoren: Kyung Seok Han Susan Ettinger Alan I. So et al.

Weitere Verfasser: Kyung Seok Han Susan Ettinger Alan I. So et al.

Quelle: Oncotarget. 6:34818-34830

Schlagwörter: 0301 basic medicine, Heat-Shock Proteins/metabolism, Indoles, sunitinib, Nude, Renal Cell/pathology, Fluorescent Antibody Technique, Angiogenesis Inhibitors, Mice, Signal Transduction/drug effects, Kidney Neoplasms/pathology, glucose-regulated protein 78, Endoplasmic Reticulum Chaperone BiP, Heat-Shock Proteins, 2. Zero hunger, Microscopy, 0303 health sciences, Tumor, Microscopy, Confocal, Indoles/pharmacology, Blotting, Endoplasmic Reticulum Stress, Immunohistochemistry, Cell Hypoxia, Kidney Neoplasms, 3. Good health, Pyrroles/pharmacology, Confocal, Gene Knockdown Techniques, Female, Western, renal cell carcinoma, Physiological, Blotting, Western, Mice, Nude, Small Interfering, Stress, Transfection, Cell Line, Angiogenesis Inhibitors/pharmacology, 03 medical and health sciences, Cell Line, Tumor, Endoplasmic Reticulum Stress/drug effects, Animals, Humans, Pyrroles, endoplasmic reticulum response, eIF-2 Kinase/metabolism, Carcinoma, Renal Cell, Endoplasmic Reticulum Stress/physiology, Signal Transduction/physiology, hypoxia, Carcinoma, Xenograft Model Antitumor Assays, RNA, Cell Hypoxia/physiology

Dateibeschreibung: application/pdf

Zugangs-URL: http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=download&path%5B%5D=5397&path%5B%5D=14903
https://pubmed.ncbi.nlm.nih.gov/26472187
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741492/
http://europepmc.org/abstract/MED/26472187
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741492/
https://www.oncotarget.com/fulltext/5397
https://mdanderson.elsevierpure.com/en/publications/inhibition-of-endoplasmic-reticulum-chaperone-protein-glucose-reg
https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/156765/1/T201504510.pdf

Lipotoxic Stress Induces Pancreaticβ-Cell Apoptosis through Modulation of Bcl-2 Proteins by the Ubiquitin-Proteasome System

Autoren: Litwak, Sara A Wali, Jibran A Pappas, Evan G et al.

Quelle: J Diabetes Res
Journal of Diabetes Research, Vol 2015 (2015)
Journal of diabetes research, 2015

Schlagwörter: 0301 basic medicine, Proteasome Endopeptidase Complex, Cell Survival, Leupeptins, Palmitic Acid -- pharmacology, Palmitic Acid, Apoptosis, Diseases of the endocrine glands. Clinical endocrinology, Cell Line, Proteasome Endopeptidase Complex -- metabolism, Mice, 03 medical and health sciences, Insulin-Secreting Cells, Ubiquitin -- metabolism, Animals, Humans, Insulin-Secreting Cells -- drug effects -- metabolism, 0303 health sciences, Proto-Oncogene Proteins c-bcl-2 -- metabolism, Ubiquitin, Endoplasmic Reticulum Stress -- drug effects, Ubiquitination -- drug effects, Ubiquitination, Sciences bio-médicales et agricoles, RC648-665, Endoplasmic Reticulum Stress, Cell Survival -- drug effects, 3. Good health, Proto-Oncogene Proteins c-bcl-2, Leupeptins -- pharmacology, Apoptosis -- drug effects, Research Article

Dateibeschreibung: text/xhtml; 1 full-text file(s): application/pdf

Zugangs-URL: http://downloads.hindawi.com/journals/jdr/2015/280615.pdf
https://pubmed.ncbi.nlm.nih.gov/26064977
https://doaj.org/article/cc42862cb1e94bc789cf5a2f5e4bdf7c
https://minerva-access.unimelb.edu.au/handle/11343/261353
https://downloads.hindawi.com/journals/jdr/2015/280615.pdf
https://difusion.ulb.ac.be/vufind/Record/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/260222/Details
https://www.ncbi.nlm.nih.gov/pubmed/26064977
https://core.ac.uk/display/29448756
https://minerva-access.unimelb.edu.au/bitstream/handle/11343/261353/PMC4438180.pdf
http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/260222