T-Cell-Specific Deletion of Map3k1 Reveals the Critical Role for Mekk1 and Jnks in Cdkn1b-Dependent Proliferative Expansion

被引：17

作者：

Suddason, Tesha ^{[1
]}

Anwar, Saba ^{[1
]}

Charlaftis, Nikolaos ^{[1
]}

Gallagher, Ewen ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Dept Med, Du Cane Rd, London W12 0NN, England

来源：

CELL REPORTS | 2016年 / 14卷 / 03期

基金：

英国惠康基金;

关键词：

NF-KAPPA-B; NKT CELLS; LIGASE ITCH; ACTIVATION; MICE; GENE; INFLAMMATION; RECOGNITION; LYMPHOCYTES; KINASES;

D O I：

10.1016/j.celrep.2015.12.047

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

MAPK signaling is important for T lymphocyte development, homeostasis, and effector responses. To better understand the role of Mekk1 (encoded by Map3k1) in T cells, we conditionally deleted Map3k1 in Lck(Cre/+) Map3k1(f/f) mice, and these display larger iNKT cell populations within the liver, spleen, and bone marrow. Mekk1 signaling controls splenic and liver iNKT cell expansion in response to glycolipid antigen. Lck(Cre/+) Map3k1(f/f) mice have enhanced liver damage in response to glycolipid antigen. Mekk1 regulates Jnk activation in iNKT cells and binds and transfers Lys63-linked poly-ubiquitin onto Carma1. Map3k1 is critical for the regulation of p27(Kip1) (encoded by Cdkn1b).

引用

页码：449 / 457

页数：9

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