https://transhumanist.ru/index.php?action=history&feed=atom&title=CHSY1 2026-10-22T20:19:16Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=CHSY1&diff=6213&oldid=prev 2021-05-12T15:17:19Z

<p>Новая страница: «Chondroitin sulfate synthase 1 (EC 2.4.1.175) (EC 2.4.1.226) (Chondroitin glucuronyltransferase 1) (Chondroitin synthase 1) (ChSy-1) (Glucuronosyl-N-acetylgalacto...»</p> <p><b>Новая страница</b></p><div>Chondroitin sulfate synthase 1 (EC 2.4.1.175) (EC 2.4.1.226) (Chondroitin glucuronyltransferase 1) (Chondroitin synthase 1) (ChSy-1) (Glucuronosyl-N-acetylgalactosaminyl-proteoglycan 4-beta-N-acetylgalactosaminyltransferase 1) (N-acetylgalactosaminyl-proteoglycan 3-beta-glucuronosyltransferase 1) (N-acetylgalactosaminyltransferase 1) [CHSY] [CSS1] [KIAA0990] [UNQ756/PRO1487]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Loss of Chondroitin Sulfate Modification Causes Inflammation and Neurodegeneration in [i]skt[/i] Mice.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31754016<br /> |abstract=One major aspect of the aging process is the onset of chronic, low-grade inflammation that is highly associated with age-related diseases. The molecular mechanisms that regulate these processes have not been fully elucidated. We have identified a spontaneous mutant mouse line, small with kinky tail ([i]skt[/i]), that exhibits accelerated aging and age-related disease phenotypes including increased inflammation in the brain and retina, enhanced age-dependent retinal abnormalities including photoreceptor cell degeneration, neurodegeneration in the hippocampus, and reduced lifespan. By positional cloning, we identified a deletion in chondroitin sulfate synthase 1 ([i]Chsy1[/i]) that is responsible for these phenotypes in [i]skt[/i] mice. [[CHSY1]] is a member of the chondroitin N-acetylgalactosaminyltransferase family that plays critical roles in the biosynthesis of chondroitin sulfate, a glycosaminoglycan (GAG) that is attached to the core protein to form the chondroitin sulfate proteoglycan (CSPG). Consistent with this function, the [i]Chsy1[/i] mutation dramatically decreases chondroitin sulfate GAGs in the retina and hippocampus. In addition, macrophage and neutrophil populations appear significantly altered in the bone marrow and spleen of [i]skt[/i] mice, suggesting an important role for [[CHSY1]] in the functioning of these immune cell types. Thus, our study reveals a previously unidentified impact of [[CHSY1]] in the retina and hippocampus. Specifically, chondroitin sulfate (CS) modification of proteins by [[CHSY1]] appears critical for proper regulation of immune cells of the myeloid lineage and for maintaining the integrity of neuronal tissues, since a defect in this gene results in increased inflammation and abnormal phenotypes associated with age-related diseases.<br /> |mesh-terms=* Age Factors<br /> * Animals<br /> * Apoptosis<br /> * Chondroitin Sulfates<br /> * Female<br /> * Glucuronosyltransferase<br /> * Inflammation<br /> * Male<br /> * Mice<br /> * Mice, Inbred C57BL<br /> * Mice, Knockout<br /> * Multifunctional Enzymes<br /> * Mutation<br /> * N-Acetylgalactosaminyltransferases<br /> * Neurodegenerative Diseases<br /> * Neurons<br /> * Protein Processing, Post-Translational<br /> * Proteins<br /> * Retinal Degeneration<br /> |keywords=* aging<br /> * chondroitin sulfate synthase<br /> * hippocampus<br /> * inflammation<br /> * mouse<br /> * myeloid cells<br /> * neurodegeneration<br /> * retina<br /> * retinal pigment epithelium<br /> * subretinal space<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6944401<br /> }}</div>

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