https://transhumanist.ru/index.php?action=history&feed=atom&title=SV2B 2026-04-12T04:35:31Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=SV2B&diff=4182&oldid=prev 2021-04-29T19:05:01Z

<p>Новая страница: «Synaptic vesicle glycoprotein 2B [KIAA0735] ==Publications== {{medline-entry |title=Mutant Huntingtin Causes a Selective Decrease in the Expression of Synaptic...»</p> <p><b>Новая страница</b></p><div>Synaptic vesicle glycoprotein 2B [KIAA0735]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Mutant Huntingtin Causes a Selective Decrease in the Expression of Synaptic Vesicle Protein 2C.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29713895<br /> |abstract=Huntington&#039;s disease (HD) is a neurodegenerative disease caused by a polyglutamine expansion in the huntingtin (Htt) protein. Mutant Htt causes synaptic transmission dysfunctions by interfering in the expression of synaptic proteins, leading to early HD symptoms. Synaptic vesicle proteins 2 (SV2s), a family of synaptic vesicle proteins including 3 members, [[SV2A]], [[SV2B]], and [[SV2C]], plays important roles in synaptic physiology. Here, we investigated whether the expression of SV2s is affected by mutant Htt in the brains of HD transgenic ([[TG]]) mice and Neuro2a mouse neuroblastoma cells (N2a cells) expressing mutant Htt. Western blot analysis showed that the protein levels of [[SV2A]] and [[SV2B]] were not significantly changed in the brains of HD [[TG]] mice expressing mutant Htt with 82 glutamine repeats. However, in the [[TG]] mouse brain there was a dramatic decrease in the protein level of [[SV2C]], which has a restricted distribution pattern in regions particularly vulnerable in HD. Immunostaining revealed that the immunoreactivity of [[SV2C]] was progressively weakened in the basal ganglia and hippocampus of [[TG]] mice. RT-PCR demonstrated that the mRNA level of [[SV2C]] progressively declined in the [[TG]] mouse brain without detectable changes in the mRNA levels of [[SV2A]] and [[SV2B]], indicating that mutant Htt selectively inhibits the transcriptional expression of [[SV2C]]. Furthermore, we found that only [[SV2C]] expression was progressively inhibited in N2a cells expressing a mutant Htt containing 120 glutamine repeats. These findings suggest that the synaptic dysfunction in HD results from the mutant Htt-mediated inhibition of [[SV2C]] transcriptional expression. These data also imply that the restricted distribution and decreased expression of [[SV2C]] contribute to the brain region-selective pathology of HD.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Brain<br /> * Cell Line, Tumor<br /> * Gene Expression<br /> * Huntingtin Protein<br /> * Membrane Glycoproteins<br /> * Mice<br /> * Mice, Transgenic<br /> * Mutation<br /> * Nerve Tissue Proteins<br /> * RNA, Messenger<br /> * Transcription, Genetic<br /> |keywords=* Basal ganglia<br /> * Hippocampus<br /> * Huntington’s disease<br /> * Synaptic vesicle protein 2C<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6129247<br /> }}</div>

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