IndraLab

Statements



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"The knockdown of Mysm1 shifts HSCs from a quiescent state to a rapid cycle and increases their apoptosis rate, which leads to the depletion of the stem cell pool and impairs the self-renewal and lineage reconstruction abilities of Mysm1-deficient mice [13]."

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"Mechanistically, defective development of Mysm1-deficient mice correlated with altered gene transcription, increased apoptosis, and increased DNA damage in a variety of tissues, and was largely rescued by concomitant deletion of tumor suppressor p53 [38,42,43,44]."

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"Higher numbers of TUNEL-positive cells were observed in the liver of AAV9-Ctrl-treated mice compared to AAV9-Mysm1-treated mice ( Figure S11A , Supporting Information ) , confirming that MYSM1 suppresses DNA damage-induced senescence and apoptosis ."

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"Mysm1 deletion promoted NSC proliferation and apoptosis, resulting in depletion of the stem cell pool."

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"Mysm1 knockdown promotes the proliferation and increases susceptibility to apoptosis of NSCs in vitro."

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"MYSM1-deficient cells have increased p38 activation, cell cycle arrest, and increased apoptosis, presumably due to altered transcriptional activity."