https://transhumanist.ru/index.php?action=history&feed=atom&title=AKTIP 2026-04-19T17:59:16Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=AKTIP&diff=5856&oldid=prev 2021-05-12T14:56:35Z

<p>Новая страница: «AKT-interacting protein (Ft1) (Fused toes protein homolog) [FTS] ==Publications== {{medline-entry |title=Mice with reduced expression of the telomere-associated...»</p> <p><b>Новая страница</b></p><div>AKT-interacting protein (Ft1) (Fused toes protein homolog) [FTS]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Mice with reduced expression of the telomere-associated protein Ft1 develop p53-sensitive progeroid traits.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29635765<br /> |abstract=Human [[AKTIP]] and mouse Ft1 are orthologous ubiquitin E2 variant proteins involved in telomere maintenance and DNA replication. [[AKTIP]] also interacts with A- and B-type lamins. These features suggest that Ft1 may be implicated in aging regulatory pathways. Here, we show that cells derived from hypomorph Ft1 mutant (Ft1 ) mice exhibit telomeric defects and that Ft1 animals develop progeroid traits, including impaired growth, skeletal and skin defects, abnormal heart tissue, and sterility. We also demonstrate a genetic interaction between Ft1 and p53. The analysis of mice carrying mutations in both Ft1 and p53 (Ft1 ; p53 and Ft1 ; p53 ) showed that reduction in p53 rescues the progeroid traits of Ft1 mutants, suggesting that they are at least in part caused by a p53-dependent DNA damage response. Conversely, Ft1 reduction alters lymphomagenesis in p53 mutant mice. These results identify Ft1 as a new player in the aging process and open the way to the analysis of its interactions with other progeria genes using the mouse model.<br /> |mesh-terms=* Animals<br /> * Apoptosis Regulatory Proteins<br /> * Cells, Cultured<br /> * Gene Expression Profiling<br /> * Mice<br /> * Mice, Inbred C57BL<br /> * Mutation<br /> * Progeria<br /> * Proteins<br /> * Tumor Suppressor Protein p53<br /> |keywords=* AKTIP<br /> * DNA damage<br /> * aging<br /> * lamins<br /> * progeria<br /> * telomeres<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6052474<br /> }}<br /> {{medline-entry<br /> |title=The telomeric protein [[AKTIP]] interacts with A- and B-type lamins and is involved in regulation of cellular senescence.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27512140<br /> |abstract=[[AKTIP]] is a shelterin-interacting protein required for replication of telomeric DNA. Here, we show that [[AKTIP]] biochemically interacts with A- and B-type lamins and affects lamin A, but not lamin C or B, expression. In interphase cells, [[AKTIP]] localizes at the nuclear rim and in discrete regions of the nucleoplasm just like lamins. Double immunostaining revealed that [[AKTIP]] partially co-localizes with lamin B1 and lamin A/C in interphase cells, and that proper [[AKTIP]] localization requires functional lamin A. In mitotic cells, [[AKTIP]] is enriched at the spindle poles and at the midbody of late telophase cells similar to lamin B1. [[AKTIP]]-depleted cells show senescence-associated markers and recapitulate several aspects of the progeroid phenotype. Collectively, our results indicate that [[AKTIP]] is a new player in lamin-related processes, including those that govern nuclear architecture, telomere homeostasis and cellular senescence.<br /> |mesh-terms=* Adaptor Proteins, Signal Transducing<br /> * Apoptosis Regulatory Proteins<br /> * Cells, Cultured<br /> * Cellular Senescence<br /> * Gene Expression Regulation<br /> * Gene Knockdown Techniques<br /> * HeLa Cells<br /> * Humans<br /> * Lamin Type A<br /> * Lamin Type B<br /> * Mitosis<br /> * Nuclear Envelope<br /> * Telomere<br /> * Telomere Homeostasis<br /> |keywords=* cell senescence<br /> * lamin<br /> * laminopathies<br /> * nuclear lamina<br /> * progeria<br /> * telomeres<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008010<br /> }}</div>

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