https://transhumanist.ru/index.php?action=history&feed=atom&title=RDH11 2026-11-10T01:31:22Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=RDH11&diff=5591&oldid=prev 2021-05-12T13:51:14Z

<p>Новая страница: «Retinol dehydrogenase 11 (EC 1.1.1.300) (Androgen-regulated short-chain dehydrogenase/reductase 1) (HCV core-binding protein HCBP12) (Prostate short-chain dehydro...»</p> <p><b>Новая страница</b></p><div>Retinol dehydrogenase 11 (EC 1.1.1.300) (Androgen-regulated short-chain dehydrogenase/reductase 1) (HCV core-binding protein HCBP12) (Prostate short-chain dehydrogenase/reductase 1) (Retinal reductase 1) (RalR1) (Short chain dehydrogenase/reductase family 7C member 1) [ARSDR1] [PSDR1] [SDR7C1] [CGI-82]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Retinol dehydrogenases [[RDH11]] and [[RDH12]] in the mouse retina: expression levels during development and regulation by oxidative stress.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/18326732<br /> |abstract=[[RDH11]] and [[RDH12]] are closely related retinol dehydrogenases expressed in the retina. [[RDH12]] has been linked to the early-onset retinal dystrophy Leber congenital amaurosis, whereas [[RDH11]] has not been associated with human disease. To understand their physiological roles, the authors investigated their expression during development and their regulation by light-induced oxidative stress in mouse retina. Quantitative RT-PCR and immunoblot analysis were used for quantification of [[RDH11]] and [[RDH12]] during development and oxidative stress. Expression during development was measured between embryonic day (E) 12 and postnatal day (P) 210 (7 months) in C57BL/6 mouse eyes. Expression during light-induced oxidative stress was measured between 2 and 24 hours of exposure to light in BALB/c mouse retina. The [[RDH11]] level was low and remarkably constant during development and oxidative stress. [[RDH12]] expression started at P7 and increased until P30 to approximately sevenfold higher than [[RDH11]]. Oxidative stress induced by exposure to constant bright light led to a rapid and significant decrease of [[RDH12]] protein. The low and constant expression of [[RDH11]] suggested a housekeeping function for this enzyme. The onset of [[RDH12]] expression during the maturation of photoreceptor cells suggested a function related to the visual process. The light-induced rapid decrease of [[RDH12]] protein, preceding the decrease of the mRNA, suggested a specific degradation of the protein rather than a regulation of gene expression.<br /> |mesh-terms=* Aging<br /> * Alcohol Oxidoreductases<br /> * Animals<br /> * Gene Expression Regulation, Developmental<br /> * Immunoblotting<br /> * In Situ Hybridization<br /> * Light<br /> * Mice<br /> * Mice, Inbred BALB C<br /> * Mice, Inbred C57BL<br /> * Mice, Knockout<br /> * Oxidative Stress<br /> * Oxidoreductases<br /> * RNA, Messenger<br /> * Radiation Injuries, Experimental<br /> * Retina<br /> * Retinal Degeneration<br /> * Retinal Dehydrogenase<br /> * Reverse Transcriptase Polymerase Chain Reaction<br /> * Transcription, Genetic<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2366097<br /> }}<br /> {{medline-entry<br /> |title=Functional characterization of mouse [[RDH11]] as a retinol dehydrogenase involved in dark adaptation in vivo.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15790565<br /> |abstract=We previously cloned mouse [[RDH11]] (m[[RDH11]]) as a gene regulated by the transcription factor sterol regulatory element-binding proteins and showed that it is a retinol dehydrogenase expressed in non-ocular tissues such as the liver and testis and in the retina (Kasus-Jacobi, A., Ou, J., Bashmakov, Y. K., Shelton, J. M., Richardson, J. A., Goldstein, J. L., and Brown, M. S. (2003) J. Biol. Chem. 278, 32380-32389). It was proposed to function in the recycling of the visual chromophore 11-cis-retinal after photoisomerization by a bleaching light, a pathway referred to as the visual cycle. In this work, we describe our studies on the ocular function of m[[RDH11]]. We created a knockout mouse by replacing the mrdh11 coding sequence with the lacZ reporter gene for expression profiling. 5-Bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X-Gal) staining demonstrated active transcription of this gene in photoreceptor cells. We show by immunoblot analysis that m[[RDH11]] is associated with retinal membranes purified from a non-outer segment fraction of the retina. No obvious retinal defect was found during development and aging of [[RDH11]]-deficient mice. The functional consequences of m[[RDH11]] disruption were investigated by electroretinography. Dark adaptation was delayed by a factor of 2.5-3 compared with wild-type mice. However, the kinetics of 11-cis-retinal recycling during dark adaptation was not affected, suggesting that m[[RDH11]] is not involved in the visual cycle. We propose that m[[RDH11]] disruption affects retinoid metabolism in photoreceptor inner segments and delays the kinetics of dark adaptation through modulation of calcium homeostasis.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Calcium<br /> * Chromatography, High Pressure Liquid<br /> * DNA<br /> * Dark Adaptation<br /> * Drug Resistance<br /> * Electroretinography<br /> * Female<br /> * Gene Expression<br /> * Gene Expression Profiling<br /> * Homeostasis<br /> * Immunoblotting<br /> * Kinetics<br /> * Liver<br /> * Male<br /> * Mice<br /> * Mice, Knockout<br /> * Neomycin<br /> * Oxidoreductases<br /> * RNA, Messenger<br /> * Retina<br /> * Retinal Rod Photoreceptor Cells<br /> * Retinoids<br /> * Testis<br /> * Transcription, Genetic<br /> * beta-Galactosidase<br /> <br /> |full-text-url=https://sci-hub.do/10.1074/jbc.M413789200<br /> }}</div>

OdysseusBot