53BP1 pathway therefore comprises distinct double-strand break repair activities within chromatin and single-stranded DNA compartments which explains both the immunological differences between 53bp1- and Rev7- deficient mice and the context specificity of the pathway
This study demonstrates using super-resolution microscopy that numerous MAD2L2 microfoci are exclusively associated with euchromatin similar to other factors of the DNA damage response. In the absence of MAD2L2 the amount of heterochromatin demarcated by H3K9me2 was significantly increased.
Skp2 a confirmed APC/C-CDH1 substrate and E-cadherin destroyer was increased in TGF-beta1-treated proximal tubular epithelial cells which could be blocked by MAD2B depletion.
Increased gonadotropins caused by the absence of functional oocytes and accumulation of DNA damage in cells caused by the lack of repair function could be responsible for the development and progression of ovarian tumors in the Rev7 mutant mouse.
the Mad2l2 (MAD2B Rev7) gene product is not only required by PGCs but also by pluripotent embryonic stem cells (ESCs) depending on the growth conditions.
results reveal an unexpected crucial function of REV7 downstream of 53BP1 in coordinating pathological DSB repair pathway choices in BRCA1-deficient cells
that MAD2B may play an important role in high glucose-mediated podocyte injury of diabetic nephropathy via modulation of Cdh1 cyclin B1 and Skp2 expression
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