Blonska Marzenna, Lin Xin
Department of Molecular and Cellular Oncology, University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Immunol Rev. 2009 Mar;228(1):199-211. doi: 10.1111/j.1600-065X.2008.00749.x.
Activation of transcription factor nuclear factor-kappaB (NF-kappaB) 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-kappaB 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-kappaB and JNK activation. In this review, we summarize our findings in revealing the roles of CARMA1 in the NF-kappaB and JNK signaling pathways in the context of recent advances in this field.
转录因子核因子-κB（NF-κB）和Jun氨基末端激酶（JNK）的激活在淋巴细胞激活和增殖的调节中起关键作用。这些信号通路的失调会导致不适当的免疫反应，并促进白血病/淋巴瘤的发展。支架蛋白CARMA1[半胱天冬酶招募结构域（CARD）膜相关鸟苷酸激酶（MAGUK）蛋白1]在B淋巴细胞和T淋巴细胞中对NF-κB以及JNK2/c-Jun复合物的调节中起核心作用。在过去几年中，人们开展了大量工作来揭示CARMA1及其信号伴侣B细胞CLL淋巴瘤10和黏膜相关淋巴组织1被激活并介导NF-κB和JNK激活的机制。在这篇综述中，我们结合该领域的最新进展，总结我们在揭示CARMA1在NF-κB和JNK信号通路中的作用方面的研究发现。
