Nucleolar protein CSIG is required for p33ING1 function in UV-induced apoptosis

作者：N Li, Gexin Zhao, T Chen, Lixiang Xue, Liantao Ma, Jing Niu, Tan Jun Tong · 发表于：Cell Death and Disease · 年份：2012 · DOI：10.1038/cddis.2012.22 · 被引用次数：45 · 研究领域：Redox biology and oxidative stress、interferon and immune responses、Cancer-related Molecular Pathways

Cellular senescence-inhibited gene (CSIG) protein, a nucleolar protein with a ribosomal L1 domain in its N-terminus, can exert non-ribosomal functions to regulate biological processes, such as cellular senescence. Here, we describe a previously unknown function for CSIG: promotion of apoptosis in response to ultraviolet (UV) irradiation-induced CSIG upregulation. We identified p33ING1 as a binding partner that interacts with CSIG. After UV irradiation, p33ING1 increases its protein expression, translocates into the nucleolus and binds CSIG. p33ING1 requires its nucleolar targeting sequence region to interact with CSIG and enhance CSIG protein stability, which is essential for activation of downstream effectors, Bcl-2-associated X protein, to promote apoptosis. Thus, our data imply that p33ING1-CSIG axis functions as a novel pro-apoptotic regulator in response to DNA damage.