肿瘤抑制因子介导的信号和疾病

Title:CYLD-Mediated Signaling and Diseases

Volume: 16 Issue: 4

Author(s): Bryan J. Mathis, Yimu Lai, Chen Qu, Joseph S. Janicki and Taixing Cui

Affiliation:

关键词: 心血管；肿瘤抑制因子；圆柱瘤；去泛素化；K63位；丝裂原活化蛋白激酶；核因子kB

摘要: The conserved cylindromatosis (CYLD) codes for a deubiquitinating enzyme and is a crucial regulator of diverse cellular processes such as immune responses, inflammation, death, and proliferation. It directly regulates multiple key signaling cascades, such as the Nuclear Factor kappa B [NFkB] and the Mitogen-Activated Protein Kinase (MAPK) pathways, by its catalytic activity on polyubiquitinated key intermediates. Several lines of emerging evidence have linked CYLD to the pathogenesis of various maladies, including cancer, poor infection control, lung fibrosis, neural development, and now cardiovascular dysfunction. While CYLD-mediated signaling is cell type and stimuli specific, the activity of CYLD is tightly controlled by phosphorylation and other regulators such as Snail. This review explores a broad selection of current and past literature regarding CYLD’s expression, function and regulation with emerging reports on its role in cardiovascular disease.

Cite this article as:

Bryan J. Mathis, Yimu Lai, Chen Qu, Joseph S. Janicki and Taixing Cui , CYLD-Mediated Signaling and Diseases, Current Drug Targets 2015; 16 (4) . https://dx.doi.org/10.2174/1389450115666141024152421