https://transhumanist.ru/index.php?action=history&feed=atom&title=NSMCE2 2026-06-04T22:02:22Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=NSMCE2&diff=4515&oldid=prev 2021-04-29T19:21:47Z

<p>Новая страница: «E3 SUMO-protein ligase NSE2 (EC 2.3.2.-) (E3 SUMO-protein transferase NSE2) (MMS21 homolog) (hMMS21) (Non-structural maintenance of chromosomes element 2 homolog)...»</p> <p><b>Новая страница</b></p><div>E3 SUMO-protein ligase NSE2 (EC 2.3.2.-) (E3 SUMO-protein transferase NSE2) (MMS21 homolog) (hMMS21) (Non-structural maintenance of chromosomes element 2 homolog) (Non-SMC element 2 homolog) [C8orf36] [MMS21]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=[[NSMCE2]] suppresses cancer and aging in mice independently of its SUMO ligase activity.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26443207<br /> |abstract=The SMC5/6 complex is the least understood of SMC complexes. In yeast, smc5/6 mutants phenocopy mutations in sgs1, the [[BLM]] ortholog that is deficient in Bloom&#039;s syndrome (BS). We here show that [[NSMCE2]] (Mms21, in Saccharomyces cerevisiae), an essential SUMO ligase of the SMC5/6 complex, suppresses cancer and aging in mice. Surprisingly, a mutation that compromises [[NSMCE2]]-dependent SUMOylation does not have a detectable impact on murine lifespan. In contrast, [[NSMCE2]] deletion in adult mice leads to pathologies resembling those found in patients of BS. Moreover, and whereas [[NSMCE2]] deletion does not have a detectable impact on DNA replication, [[NSMCE2]]-deficient cells also present the cellular hallmarks of BS such as increased recombination rates and an accumulation of micronuclei. Despite the similarities, [[NSMCE2]] and [[BLM]] foci do not colocalize and concomitant deletion of Blm and Nsmce2 in B lymphocytes further increases recombination rates and is synthetic lethal due to severe chromosome mis-segregation. Our work reveals that SUMO- and [[BLM]]-independent activities of [[NSMCE2]] limit recombination and facilitate segregation; functions of the SMC5/6 complex that are necessary to prevent cancer and aging in mice. <br /> |mesh-terms=* Aging<br /> * Animals<br /> * B-Lymphocytes<br /> * Base Sequence<br /> * Cells, Cultured<br /> * Chromosome Segregation<br /> * DNA Breaks, Double-Stranded<br /> * DNA Mutational Analysis<br /> * DNA Replication<br /> * Female<br /> * Haploinsufficiency<br /> * Humans<br /> * Ligases<br /> * Mice, 129 Strain<br /> * Mice, Inbred C57BL<br /> * Mice, Knockout<br /> * Neoplasms<br /> * Protein Transport<br /> * RecQ Helicases<br /> * Sumoylation<br /> * Tumor Suppressor Proteins<br /> * Ubiquitin-Protein Ligases<br /> |keywords=* NSMCE2<br /> * SMC5/6<br /> * SUMO<br /> * chromosome segregation<br /> * mouse models<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4641528<br /> }}</div>

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