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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, N. Zhao, G. Chen, T. Xue, L. Ma, L. Niu, J. Tong, T.
Description	Author Affiliation: Li N ( Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, People's Republic of China.)
Abstract	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.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2012.22
Journal	Cell Death and Disease
Volume Number	3
Language	English
Publisher	Nature Publishing Group
Publisher Date	2012-03-15
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Cell Nucleolus Research Support, Non-u.s. Gov't Intracellular Signaling Peptides And Proteins Dna Damage Pregnancy Proteins Hek293 Cells Transfection Ultraviolet Rays Bcl-2-associated X Protein Genetics Binding Sites Gene Expression Signal Transduction Metabolism Nuclear Proteins Protein Transport Discipline Cell Biology Up-regulation Radiation Effects Protein Binding Tumor Suppressor Proteins Hela Cells Apoptosis Ribosomal Proteins
Content Type	Text
Resource Type	Article

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