Linked Life Data

20015864

Source:http://linkedlifedata.com/resource/pubmed/id/20015864

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pubmed-article:20015864pubmed:abstractTextThe acidic leucine-rich nuclear phosphoprotein 32 (ANP32)B has been reported to regulate gene expression by acting as a histone chaperone or modulate messenger RNA trafficking by serving as a HuR ligand. However, its exact cellular functions are poorly understood. By utilizing a proteomics-based approach, in this work, we identify that the human ANP32B protein is cleaved during apoptosis induction by NSC606985, a novel camptothecin analog. Further investigation shows that various apoptosis inducers cause a decrease of full-length ANP32B in multiple cell lines with a concomitant increase of an approximately 17 kDa fragment. The proteolytic cleavage of ANP32B is inhibited by a specific caspase-3 inhibitor Z-DEVD-fmk, and it cannot be seen in NSC606985-induced death of caspase-3-deficient MCF-7 cells. In vitro caspase cleavage assay and mutagenesis experiment reveal that ANP32B is a direct substrate of caspase-3 and it is primarily cleaved at the sequence of Ala-Glu-Val-Asp, after Asp-163. Additionally, the reduced expression of endogenous ANP32B by specific small interfering RNA enhances caspase-3 activation and apoptosis induction by NSC606985 and etoposide. These results suggest that ANP32B is a novel substrate for caspase-3 and acts as a negative regulator for apoptosis, the mechanism of which remains to be explored.lld:pubmed
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pubmed-article:20015864pubmed:authorpubmed-author:ChenGuo-Qiang...lld:pubmed
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pubmed-article:20015864pubmed:articleTitleDownregulation of ANP32B, a novel substrate of caspase-3, enhances caspase-3 activation and apoptosis induction in myeloid leukemic cells.lld:pubmed
pubmed-article:20015864pubmed:affiliationInstitute of Health Science, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences-Shanghai Jiao-Tong University School of Medicine, No. 280, Chong-Qing South Road, Shanghai 200025, China.lld:pubmed
pubmed-article:20015864pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20015864pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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