anti-Harakiri, BCL2 Interacting Protein (Contains Only BH3 Domain) (HRK) 抗体

Human Harakiri, BCL2 Interacting Protein (Contains Only BH3 Domain) (HRK) interaction partners

1. 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.

2. 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.

3. 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.

4. 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.

5. Diva binds peptides derived from the BH3 domain of several other proapoptotic Bcl-2 proteins, including mouse Harakiri, Bid, Bak and Bmf.

6. The BH3-only protein harakiri (HRK) is transactivated by ATF4 in severe hypoxia through direct binding of ATF4 to the promoter region.

7. 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.

8. These results are used to propose a tentative structural model of how Harakiri works.

9. analysis of a novel interaction between Bcl-2 members Diva and Harakiri

10. Hrk is involved in the induction of apoptosis in RGCs after optic nerve transection.

11. apoptosis inducers as diverse as oncoprotein inhibitors and cell death receptor activators trigger Hrk expression via blockade of DREAM in leukemia cells

12. Data report that human oocytes and fragmenting preimplantation embryos possess transcripts encoding Harakiri and caspase-3.

13. HRK is a target of epigenetic inactivation in colorectal and gastric cancer

14. 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.

15. 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

16. in response to PAHs, Ahr-mediated activation of the harakiri, BCL2 interacting protein (contains only BH3 domain), was necessary for execution of cell death.

17. 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.

Mouse (Murine) Harakiri, BCL2 Interacting Protein (Contains Only BH3 Domain) (HRK) interaction partners

1. Hrk deficiency does not significantly attenuate the widespread apoptosis seen in the Bcl-x (-/-) embryonic nervous system, indicating that other BH3-only molecules, alone or in combination, may regulate BAX activation in immature neurons.

2. DP5 plays an important role in neuronal cell death induced by axotomy and NGF deprivation through the regulation of mitochondrial function and caspase-3 activation

3. These results demonstrate that HRK contributes to apoptosis signalling elicited by trophic factor withdrawal in certain neuronal populations but is dispensable for apoptosis of haematopoietic cells.

4. in response to PAHs, Ahr-mediated activation of the harakiri, BCL2 interacting protein (contains only BH3 domain), was necessary for execution of cell death.

5. The effect of antisense oligonucleoties specific to the harakiri mRNA on spontaneous and induced defects of mouse preimplantation embryo development