https://transhumanist.ru/index.php?action=history&feed=atom&title=FLNA 2026-06-04T14:25:35Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=FLNA&diff=6571&oldid=prev 2021-05-12T15:37:44Z

<p>Новая страница: «Filamin-A (FLN-A) (Actin-binding protein 280) (ABP-280) (Alpha-filamin) (Endothelial actin-binding protein) (Filamin-1) (Non-muscle filamin) [FLN] [FLN1] ==Publi...»</p> <p><b>Новая страница</b></p><div>Filamin-A (FLN-A) (Actin-binding protein 280) (ABP-280) (Alpha-filamin) (Endothelial actin-binding protein) (Filamin-1) (Non-muscle filamin) [FLN] [FLN1]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=[[SQSTM1]]/p62 mediates crosstalk between autophagy and the UPS in DNA repair.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27391408<br /> |abstract=[[SQSTM1]]/p62 (sequestosome 1) selectively targets polyubiquitinated proteins for degradation via macroautophagy and the proteasome. Additionally, [[SQSTM1]] shuttles between the cytoplasmic and nuclear compartments, although its role in the nucleus is relatively unknown. Here, we report that [[SQSTM1]] dynamically associates with DNA damage foci (DDF) and regulates DNA repair. Upon induction of DNA damage [[SQSTM1]] interacts with [[FLNA]] (filamin A), which has previously been shown to recruit DNA repair protein [[RAD51]] ([[RAD51]] recombinase) to double-strand breaks and facilitate homologous recombination ([[HR]]). [[SQSTM1]] promotes proteasomal degradation of [[FLNA]] and [[RAD51]] within the nucleus, resulting in reduced levels of nuclear [[RAD51]] and slower DNA repair. [[SQSTM1]] regulates the ratio between [[HR]] and nonhomologous end joining (NHEJ) by promoting the latter at the expense of the former. This [[SQSTM1]]-dependent mechanism mediates the effect of macroautophagy on DNA repair. Moreover, nuclear localization of [[SQSTM1]] and its association with DDF increase with aging and are prevented by life-span-extending dietary restriction, suggesting that an imbalance in the mechanism identified here may contribute to aging and age-related diseases.<br /> |mesh-terms=* Animals<br /> * Autophagy<br /> * Cell Nucleus<br /> * DNA Damage<br /> * DNA Repair<br /> * Filamins<br /> * Kinetics<br /> * Mice, Inbred C57BL<br /> * Models, Biological<br /> * Proteasome Endopeptidase Complex<br /> * Protein Transport<br /> * Proteolysis<br /> * Rad51 Recombinase<br /> * Sequestosome-1 Protein<br /> * Ubiquitin<br /> |keywords=* DNA damage<br /> * SQSTM1<br /> * aging<br /> * autophagy<br /> * homologous recombination<br /> * nonhomologous end joining<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391493<br /> }}</div>

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