CNOT3 contributes to early B cell development by controlling Igh rearrangement and p53 mRNA stability

Takeshi Inoue,M. Morita,A. Hijikata,Yoko Fukuda-Yuzawa,S. Adachi,K. Isono,T. Ikawa,H. Kawamoto,H. Koseki,T. Natsume,T. Fukao,O. Ohara,Tadashi Yamamoto,T. Kurosaki

Published 2015 in Journal of Experimental Medicine

ABSTRACT

Inoue et al. report that CNOT3, a subunit of the CCR4–NOT deadenylase complex regulating mRNA decay and translational repression, controls Igh gene rearrangement and destabilizes the mRNA of the tumor suppressor p53. Loss of CNOT3 results in a block of pro- to pre–B cell transition.

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