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- W820165059 abstract "During immune responses, B cell repertoire is diversified through somatic hypermutation (SHM) and class switch recombination (CSR). SHM and CSR require activation-induced cytidine deaminase (AID), which induces DNA damage. While AID deficiency abrogates SHM and CSR, C-terminal truncations impair CSR without affecting SHM and it has been proposed that AID C-terminal domain associates with CSR-specific factor(s). In order to identify these factors, we studied a human CSR-specific immunodeficiency, characterized by normal SHM and AID expression. B cells from these patients do not display DSBs at switch (S) regions, suggesting that they might lack an AID-binding factor(s) required to target AID to S regions during CSR. Through a multi- approach strategy, we identified and analyzed candidate factors, including Spt6, the cohesin complex and the Smc5/6 complex. We show that, in B cells poised to undergo CSR, AID is in a complex with Spt6, Spt5, the RNA polymerase II and the PAF complex while cohesins might regulate the 3D structure of the IgH locus and the pathway of DSBs repair at the Ig S regions. Our work thus contributes to a better understanding of the CSR reaction." @default.
- W820165059 created "2016-06-24" @default.
- W820165059 creator A5036764539 @default.
- W820165059 date "2013-09-30" @default.
- W820165059 modified "2023-09-27" @default.
- W820165059 title "Molecular mechanisms controlling immunoglobulin class switch recombination" @default.
- W820165059 hasPublicationYear "2013" @default.
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