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Cornelia de Lange Syndrome as Paradigm of Chromatinopathies
Variants in the cohesin regulator NIPBL are the most frequent cause of CdLS and account for approximately 70% of cases. Other subunits or regulators of the complex (SMC1A, SMC3, RAD21, and HDAC8) are responsible altogether for 10–15% of cases ( Kline et al., 2018 ).
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Nov 01, 2013 · A regulatory role for the cohesin loader NIPBL in nonhomologous end joining during immunoglobulin class switch recombination Published in The Journal of Experimental Medicine, 210(12), 2503 - 2513.
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(PDF) Regulation of the cohesin-loading factor NIPBL: Role
Cohesin is crucial for genome stability, cell division, transcription and chromatin organization. Its functions critically depend on NIPBL, the cohesin-loader protein that is found to be mutated in >60% of the cases of Cornelia de Lange syndrome
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Regulation of the cohesin-loading factor NIPBL: Role of
Thus, NIPBL may regulate NHEJ by recruiting 53BP1 to the DSB sites, but it is likely that interactions between NIPBL and the DNA damage response factors are complex and that factors in addition to 53PB1 may also influence the function of NIPBL in NHEJ. Given that cohesin and NIPBL have been shown to regulate gene expression, an indirect effect caused by …
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