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. Author manuscript; available in PMC: 2012 May 17.
Published in final edited form as: Cancer Cell. 2011 May 17;19(5):569–570. doi: 10.1016/j.ccr.2011.05.002

Figure 1. ATMIN is a tumor suppressor in developing B cells.

Figure 1

B cell development requires sequential modifications of the antigen receptor loci through V(D)J recombination and CSR. Both V(D)J recombination and CSR generate DNA DSBs and involve chromatin changes, which activates ATM and lead to the phosphorylation of ATM substrates. ATMIN potentially contributes to DNA repair and checkpoint control in developing B cells [I] as an activator of ATM in response to chromatin changes; [II] as a substrate of ATM and [III] independent of ATM. Together ATMIN deficiency leads to genomic instability and B cell lymphomas.