CARMA1-mediated NF-κB and JNK activation in lymphocytes

被引:87
作者
Blonska, Marzenna [1 ]
Lin, Xin [1 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA
基金
美国国家卫生研究院;
关键词
NF-kappa B; IKK; JNK; Jun; AP-1; CARMA1; CASPASE RECRUITMENT DOMAIN; CELL ANTIGEN RECEPTOR; KINASE-C-THETA; T-CELL; UBIQUITIN LIGASE; SIGNAL-TRANSDUCTION; INDUCED PHOSPHORYLATION; TRANSCRIPTION FACTOR; NEGATIVE REGULATOR; PARACASPASE MALT1;
D O I
10.1111/j.1600-065X.2008.00749.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Activation of transcription factor nuclear factor-kappa B (NF-kappa B) and Jun N-terminal kinase (JNK) play the pivotal roles in regulation of lymphocyte activation and proliferation. Deregulation of these signaling pathways leads to inappropriate immune response and contributes to the development of leukemia/lymphoma. The scaffold protein CARMA1 [caspase-recruitment domain (CARD) membrane-associated guanylate kinase (MAGUK) protein 1] has a central role in regulation of NF-kappa B and the JNK2/c-Jun complex in both B and T lymphocytes. During last several years, tremendous work has been done to reveal the mechanism by which CARMA1 and its signaling partners, B cell CLL-lymphoma 10 and mucosa-associated lymphoid tissue 1, are activated and mediate NF-kappa B and JNK activation. In this review, we summarize our findings in revealing the roles of CARMA1 in the NF-kappa B and JNK signaling pathways in the context of recent advances in this field.
引用
收藏
页码:199 / 211
页数:13
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