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Map3k1在T细胞中的特异性缺失揭示了Mekk1和Jnk在依赖Cdkn1b的增殖性扩张中的关键作用。

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

作者信息

Suddason Tesha, Anwar Saba, Charlaftis Nikolaos, Gallagher Ewen

机构信息

Department of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.

Department of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK.

出版信息

Cell Rep. 2016 Jan 26;14(3):449-457. doi: 10.1016/j.celrep.2015.12.047. Epub 2016 Jan 7.

DOI:10.1016/j.celrep.2015.12.047
PMID:26774476
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4733086/
Abstract

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).

摘要

丝裂原活化蛋白激酶（MAPK）信号传导对于T淋巴细胞的发育、稳态和效应反应至关重要。为了更好地理解Mekk1（由Map3k1编码）在T细胞中的作用，我们在Lck(Cre/+)Map3k1(f/f)小鼠中条件性敲除Map3k1，这些小鼠在肝脏、脾脏和骨髓中表现出更大的不变自然杀伤T（iNKT）细胞群体。Mekk1信号传导控制脾脏和肝脏中iNKT细胞对糖脂抗原的反应性扩张。Lck(Cre/+)Map3k1(f/f)小鼠对糖脂抗原的反应导致肝脏损伤增强。Mekk1调节iNKT细胞中的Jnk活化，并将K63连接的多聚泛素结合并转移到Carma1上。Map3k1对于p27(Kip1)（由Cdkn1b编码）的调节至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/2e7e53538a94/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/40179ec79c1d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/d127845518aa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/caf8ad18a66b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/df99e81d1ef2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/e571a4d9df3f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/2e7e53538a94/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/40179ec79c1d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/d127845518aa/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/caf8ad18a66b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/df99e81d1ef2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/e571a4d9df3f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1079/4733086/2e7e53538a94/gr5.jpg

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