Редактирование: ATMIN (раздел)

==Publications==

{{medline-entry
|title=Perturbed hematopoiesis in mice lacking [[ATM]]IN.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27581360
|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.
|mesh-terms=* Aging
* Animals
* Apoptosis
* Ataxia Telangiectasia Mutated Proteins
* B-Lymphocytes
* Chronic Disease
* Gene Deletion
* Hematopoiesis
* Hematopoietic Stem Cells
* Leukopenia
* Mice
* Mice, Knockout
* Oxidative Stress
* Transcription Factors

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5147016
}}