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The apoptosis phenotype was partly dependent on HRK upregulation, as HRK knockdown significantly abrogated the sensitization. KDM2B-silenced tumors exhibited slower growth in vivo. Taken together, our findings suggest a novel mechanism, where the key apoptosis components are under epigenetic control of KDM2B in glioblastoma multiforme cells.
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miR-23a-3p, miR-23b-3p, and miR-149-5p, were downregulated by cytokines and selected for further studies. These miRNAs were found to regulate the expression of the proapoptotic Bcl-2 proteins DP5 and PUMA and consequent human beta-cell apoptosis.
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our findings suggest that induction of the BH3-only protein Hrk is a critical step in 2-ME activation of the JNK-induced apoptotic pathway, targeting mitochondria by liberating proapoptotic protein Bak.
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SUZ12 promotes the proliferation of human EOC cells by inhibiting apoptosis and HRK is a novel SUZ12 target gene whose upregulation contributes to apoptosis induced by SUZ12 knockdown.
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Diva binds peptides derived from the BH3 domain of several other proapoptotic Bcl-2 proteins, including mouse Harakiri, Bid, Bak and Bmf.
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The BH3-only protein harakiri (HRK) is transactivated by ATF4 in severe hypoxia through direct binding of ATF4 to the promoter region.
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Data suggest that DP5 and PUMA/BBC3 (p53 up-regulated modulator of apoptosis/bcl-2-binding component 3) contribute to palmitate-induced apoptosis of pancreatic beta-cells via lipotoxic endoplasmic reticulum stress.
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These results are used to propose a tentative structural model of how Harakiri works.
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analysis of a novel interaction between Bcl-2 members Diva and Harakiri
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Hrk is involved in the induction of apoptosis in RGCs after optic nerve transection.
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apoptosis inducers as diverse as oncoprotein inhibitors and cell death receptor activators trigger Hrk expression via blockade of DREAM in leukemia cells
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Data report that human oocytes and fragmenting preimplantation embryos possess transcripts encoding Harakiri and caspase-3.
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HRK is a target of epigenetic inactivation in colorectal and gastric cancer
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The interaction between HRK and cellular protein p32 was studied. HRK-induced apoptosis was suppresssed by the expression of p32 mutants lacking the N-terminal sequences 74-282 and the C-terminal sequences 1-221.
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HRK appears to be inactivated principally by promoter hypermethylation in prostate cancers and decreased expression may play an important role in tumor progression by modulating apoptotic cell death
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in response to PAHs, Ahr-mediated activation of the harakiri, BCL2 interacting protein (contains only BH3 domain), was necessary for execution of cell death.
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Aberrant 5'-CpG methylation status and loss of heterozygosity on 12q13.1 are associated with HRK expression in human malignancies, including prostate cancers, astrocytic tumors and primary central nervous system lymphomas. Review.
