https://transhumanist.ru/index.php?action=history&feed=atom&title=DLX2 2026-06-23T01:07:51Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=DLX2&diff=6390&oldid=prev 2021-05-12T15:27:58Z

<p>Новая страница: «Homeobox protein DLX-2 ==Publications== {{medline-entry |title=A gain-of-function senescence bypass screen identifies the homeobox transcription factor <a href="/DLX2" title="DLX2">DLX2</a>...»</p> <p><b>Новая страница</b></p><div>Homeobox protein DLX-2<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=A gain-of-function senescence bypass screen identifies the homeobox transcription factor [[DLX2]] as a regulator of [[ATM]]-p53 signaling.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26833729<br /> |abstract=Senescence stimuli activate multiple tumor suppressor pathways to initiate cycle arrest and a differentiation program characteristic of senescent cells. We performed a two-stage, gain-of-function screen to select for the genes whose enhanced expression can bypass replicative senescence. We uncovered multiple genes known to be involved in p53 and Rb regulation and [[ATM]] regulation, two components of the CST (CTC1-[[STN1]]-TEN1) complex involved in preventing telomere erosion, and genes such as [[REST]] and [[FOXO4]] that have been implicated in aging. Among the new genes now implicated in senescence, we identified [[DLX2]], a homeobox transcription factor that has been shown to be required for tumor growth and metastasis and is associated with poor cancer prognosis. Growth analysis showed that [[DLX2]] expression led to increased cellular replicative life span. Our data suggest that [[DLX2]] expression reduces the protein components of the TTI1/TTI2/TEL2 complex, a key complex required for the proper folding and stabilization of [[ATM]] and other members of the PIKK (phosphatidylinositol 3-kinase-related kinase) family kinase, leading to reduced [[ATM]]-p53 signaling and senescence bypass. We also found that the overexpression of [[DLX2]] exhibited a mutually exclusive relationship with p53 alterations in cancer patients. Our functional screen identified novel players that may promote tumorigenesis by regulating the [[ATM]]-p53 pathway and senescence. <br /> |mesh-terms=* Ataxia Telangiectasia Mutated Proteins<br /> * Cell Line<br /> * Cellular Senescence<br /> * Computational Biology<br /> * Gene Expression Regulation<br /> * Homeodomain Proteins<br /> * Humans<br /> * Reproducibility of Results<br /> * Signal Transduction<br /> * Telomere Homeostasis<br /> * Transcription Factors<br /> * Transcriptional Activation<br /> * Tumor Suppressor Protein p53<br /> |keywords=* ATM<br /> * genetic screen<br /> * senescence<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4743059<br /> }}</div>

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