https://transhumanist.ru/index.php?action=history&feed=atom&title=ATMIN 2026-06-14T00:17:26Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=ATMIN&diff=4271&oldid=prev 2021-04-29T19:09:33Z

<p>Новая страница: «ATM interactor (ATM/ATR-substrate CHK2-interacting zinc finger protein) (ASCIZ) (Zinc finger protein 822) [KIAA0431] [ZNF822] ==Publications== {{medline-entry |...»</p> <p><b>Новая страница</b></p><div>ATM interactor (ATM/ATR-substrate CHK2-interacting zinc finger protein) (ASCIZ) (Zinc finger protein 822) [KIAA0431] [ZNF822]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Perturbed hematopoiesis in mice lacking [[ATM]]IN.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27581360<br /> |abstract=The ataxia telangiectasia mutated ([[ATM]])-interacting protein [[ATM]]IN mediates noncanonical [[ATM]] signaling in response to oxidative and replicative stress conditions. Like [[ATM]], [[ATM]]IN can function as a tumor suppressor in the hematopoietic system: deletion of Atmin under the control of [[CD19]]-Cre results in B-cell lymphomas in aging mice. [[ATM]] signaling is essential for lymphopoiesis and hematopoietic stem cell (HSC) function; however, little is known about the role of [[ATM]]IN in hematopoiesis. We thus sought to investigate whether the absence of [[ATM]]IN would affect primitive hematopoietic cells in an [[ATM]]-dependent or -independent manner. Apart from its role in B-cell development, we show that [[ATM]]IN has an [[ATM]]-independent function in the common myeloid progenitors (CMPs) by deletion of Atmin in the entire hematopoietic system using Vav-Cre. Despite the lack of lymphoma formation, [[ATM]]IN-deficient mice developed chronic leukopenia as a result of high levels of apoptosis in B cells and CMPs and induced a compensatory mechanism in which HSCs displayed enhanced cycling. Consequently, [[ATM]]IN-deficient HSCs showed impaired regeneration ability with the induction of the DNA oxidative stress response, especially when aged. [[ATM]]IN, therefore, has multiple roles in different cell types, and its absence results in perturbed hematopoiesis, especially during stress conditions and aging.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Apoptosis<br /> * Ataxia Telangiectasia Mutated Proteins<br /> * B-Lymphocytes<br /> * Chronic Disease<br /> * Gene Deletion<br /> * Hematopoiesis<br /> * Hematopoietic Stem Cells<br /> * Leukopenia<br /> * Mice<br /> * Mice, Knockout<br /> * Oxidative Stress<br /> * Transcription Factors<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5147016<br /> }}</div>

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