Retinoid X Receptor: Cellular and Biochemical Roles of Nuclear Receptor with a Focus on Neuropathological Involvement
Retinoid X receptors (RXRs) present a subgroup of the nuclear receptor superfamily with particularly high evolutionary conservation of ligand binding domain. The receptor exists in α, β, and γ isotypes that form homo-/heterodimeric complexes with other permissive and non-permissive receptors. While...
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| Published in: | Molecular neurobiology Vol. 59; no. 4; pp. 2027 - 2050 |
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| Main Authors: | , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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New York
Springer US
01.04.2022
Springer Nature B.V Springer |
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| ISSN: | 0893-7648, 1559-1182, 1559-1182 |
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| Abstract | Retinoid X receptors (RXRs) present a subgroup of the nuclear receptor superfamily with particularly high evolutionary conservation of ligand binding domain. The receptor exists in α, β, and γ isotypes that form homo-/heterodimeric complexes with other permissive and non-permissive receptors. While research has identified the biochemical roles of several nuclear receptor family members, the roles of RXRs in various neurological disorders remain relatively under-investigated. RXR acts as ligand-regulated transcription factor, modulating the expression of genes that plays a critical role in mediating several developmental, metabolic, and biochemical processes. Cumulative evidence indicates that abnormal RXR signalling affects neuronal stress and neuroinflammatory networks in several neuropathological conditions. Protective effects of targeting RXRs through pharmacological ligands have been established in various cell and animal models of neuronal injury including Alzheimer disease, Parkinson disease, glaucoma, multiple sclerosis, and stroke. This review summarises the existing knowledge about the roles of RXR, its interacting partners, and ligands in CNS disorders. Future research will determine the importance of structural and functional heterogeneity amongst various RXR isotypes as well as elucidate functional links between RXR homo- or heterodimers and specific physiological conditions to increase drug targeting efficiency in pathological conditions. |
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| AbstractList | Retinoid X receptors (RXRs) present a subgroup of the nuclear receptor superfamily with particularly high evolutionary conservation of ligand binding domain. The receptor exists in α, β, and γ isotypes that form homo-/heterodimeric complexes with other permissive and non-permissive receptors. While research has identified the biochemical roles of several nuclear receptor family members, the roles of RXRs in various neurological disorders remain relatively under-investigated. RXR acts as ligand-regulated transcription factor, modulating the expression of genes that plays a critical role in mediating several developmental, metabolic, and biochemical processes. Cumulative evidence indicates that abnormal RXR signalling affects neuronal stress and neuroinflammatory networks in several neuropathological conditions. Protective effects of targeting RXRs through pharmacological ligands have been established in various cell and animal models of neuronal injury including Alzheimer disease, Parkinson disease, glaucoma, multiple sclerosis, and stroke. This review summarises the existing knowledge about the roles of RXR, its interacting partners, and ligands in CNS disorders. Future research will determine the importance of structural and functional heterogeneity amongst various RXR isotypes as well as elucidate functional links between RXR homo-or heterodimers and specific physiological conditions to increase drug targeting efficiency in pathological conditions. Retinoid X receptors (RXRs) present a subgroup of the nuclear receptor superfamily with particularly high evolutionary conservation of ligand binding domain. The receptor exists in α, β, and γ isotypes that form homo-/heterodimeric complexes with other permissive and non-permissive receptors. While research has identified the biochemical roles of several nuclear receptor family members, the roles of RXRs in various neurological disorders remain relatively under-investigated. RXR acts as ligand-regulated transcription factor, modulating the expression of genes that plays a critical role in mediating several developmental, metabolic, and biochemical processes. Cumulative evidence indicates that abnormal RXR signalling affects neuronal stress and neuroinflammatory networks in several neuropathological conditions. Protective effects of targeting RXRs through pharmacological ligands have been established in various cell and animal models of neuronal injury including Alzheimer disease, Parkinson disease, glaucoma, multiple sclerosis, and stroke. This review summarises the existing knowledge about the roles of RXR, its interacting partners, and ligands in CNS disorders. Future research will determine the importance of structural and functional heterogeneity amongst various RXR isotypes as well as elucidate functional links between RXR homo- or heterodimers and specific physiological conditions to increase drug targeting efficiency in pathological conditions.Retinoid X receptors (RXRs) present a subgroup of the nuclear receptor superfamily with particularly high evolutionary conservation of ligand binding domain. The receptor exists in α, β, and γ isotypes that form homo-/heterodimeric complexes with other permissive and non-permissive receptors. While research has identified the biochemical roles of several nuclear receptor family members, the roles of RXRs in various neurological disorders remain relatively under-investigated. RXR acts as ligand-regulated transcription factor, modulating the expression of genes that plays a critical role in mediating several developmental, metabolic, and biochemical processes. Cumulative evidence indicates that abnormal RXR signalling affects neuronal stress and neuroinflammatory networks in several neuropathological conditions. Protective effects of targeting RXRs through pharmacological ligands have been established in various cell and animal models of neuronal injury including Alzheimer disease, Parkinson disease, glaucoma, multiple sclerosis, and stroke. This review summarises the existing knowledge about the roles of RXR, its interacting partners, and ligands in CNS disorders. Future research will determine the importance of structural and functional heterogeneity amongst various RXR isotypes as well as elucidate functional links between RXR homo- or heterodimers and specific physiological conditions to increase drug targeting efficiency in pathological conditions. |
| Author | Shen, Ting Sharma, Samridhi Mirzaei, Mehdi Graham, Stuart L. Chitranshi, Nitin Sarkar, Soumalya You, Yuyi Basavarajappa, Devaraj Krezel, Wojciech Gupta, Veer Gupta, Vivek |
| Author_xml | – sequence: 1 givenname: Samridhi orcidid: 0000-0002-1167-6511 surname: Sharma fullname: Sharma, Samridhi email: samridhi.sharma@mq.edu.au organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University – sequence: 2 givenname: Ting surname: Shen fullname: Shen, Ting organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University – sequence: 3 givenname: Nitin surname: Chitranshi fullname: Chitranshi, Nitin organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University – sequence: 4 givenname: Veer surname: Gupta fullname: Gupta, Veer organization: School of Medicine, Deakin University – sequence: 5 givenname: Devaraj surname: Basavarajappa fullname: Basavarajappa, Devaraj organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University – sequence: 6 givenname: Soumalya surname: Sarkar fullname: Sarkar, Soumalya organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University – sequence: 7 givenname: Mehdi surname: Mirzaei fullname: Mirzaei, Mehdi organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University – sequence: 8 givenname: Yuyi surname: You fullname: You, Yuyi organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Save Sight Institute, University of Sydney – sequence: 9 givenname: Wojciech surname: Krezel fullname: Krezel, Wojciech organization: Institut de Génétique Et de Biologie Moléculaire Et Cellulaire – sequence: 10 givenname: Stuart L. surname: Graham fullname: Graham, Stuart L. organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Save Sight Institute, University of Sydney – sequence: 11 givenname: Vivek surname: Gupta fullname: Gupta, Vivek email: vivek.gupta@mq.edu.au organization: Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35015251$$D View this record in MEDLINE/PubMed https://hal.science/hal-04217983$$DView record in HAL |
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| Keywords | Lipid metabolism ligand Glaucoma Neuroprotection Bexarotene Multiple sclerosis Stroke Endogenous ligands Alzheimer disease Parkinson disease Neuroinflammation Lipid X receptor (LXR) Nuclear receptors Neuronal stress Exogenous ligands Glucose metabolism Nuclear receptor-related 1 (Nurr1) Retinoid X receptor (RXR) Peroxisome proliferator-activated receptor (PPAR) Heterodimerisation Neuroinfammation |
| Language | English |
| License | 2021. The Author(s). licence_http://creativecommons.org/publicdomain/zero/: http://creativecommons.org/publicdomain/zero Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
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| PublicationTitle | Molecular neurobiology |
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