Nucleolar protein CSIG is required for p33ING1 function in UV-induced apoptosis.
Nucleolar protein CSIG is required for p33ING1 function in UV-induced apoptosis.
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核仁蛋白 CSIG 是 p33ING1 在紫外线诱导的细胞凋亡中发挥功能所必需的
DOI：
10.1038/cddis.2012.22
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发表时间：
2012-03-15
影响因子：
9
通讯作者：
中科院分区：
文献类型：
--
作者：
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.
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