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Hrk  -  harakiri, BCL2 interacting protein...

Mus musculus

Synonyms: AI838259, Activator of apoptosis harakiri, BH3-interacting domain-containing protein 3, Bid3, DP5, ...
 
 
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High impact information on Hrk

  • In all cases, loss of the DREAM-DNA binding complex was correlated with increased levels of Hrk and apoptosis [1].
  • Deletion of 16 amino acids including the conserved BH3 region abolished the ability of Hrk to interact with Bcl-2 and Bcl-X(L) in mammalian cells [2].
  • Expression of Hrk induces cell death which is inhibited by Bcl-2 and Bcl-X(L) [2].
  • The induction of DP5 gene expression was blocked when cell death was rescued by treatment with cycloheximide, KCl, or the cyclic AMP analogue CPTcAMP [3].
  • We found no evidence that Hrk or Apaf1, and by inference the mitochondrial cell death pathway, are involved in regulating the number of neurosphere-derived progeny [4].
 

Biological context of Hrk

 

Anatomical context of Hrk

  • Analysis of SCG neurons from DP5-/- mice revealed increased preservation of mitochondrial membrane potential and reduced activation of caspase-3 compared with neurons from wild-type mice [5].
  • Notably, motoneurons from DP5-/- mice were highly protected from cell death induced by resection of the hypoglossal nerve compared with motoneurons from DP5+/+ littermate mice [5].
  • Finally, Hrk was up-regulated by TCDD in Jurkat T cells, suggesting the potential role of Hrk in thymic atrophy and the possibility of exploiting Jurkat T cells as a suitable in vitro model for studying mechanisms of thymic atrophy [6].
 

Other interactions of Hrk

  • These results indicate that 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 [5].
  • Hrk lacks conserved BH1 and BH2 regions and significant homology to Bcl-2 family members or any other protein, except for a stretch of eight amino acids that exhibits high homology with BH3 regions [2].
 

Analytical, diagnostic and therapeutic context of Hrk

References

  1. Interleukin 3-dependent activation of DREAM is involved in transcriptional silencing of the apoptotic Hrk gene in hematopoietic progenitor cells. Sanz, C., Mellstrom, B., Link, W.A., Naranjo, J.R., Fernandez-Luna, J.L. EMBO J. (2001) [Pubmed]
  2. harakiri, a novel regulator of cell death, encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L). Inohara, N., Ding, L., Chen, S., Núñez, G. EMBO J. (1997) [Pubmed]
  3. Molecular cloning of a novel polypeptide, DP5, induced during programmed neuronal death. Imaizumi, K., Tsuda, M., Imai, Y., Wanaka, A., Takagi, T., Tohyama, M. J. Biol. Chem. (1997) [Pubmed]
  4. Neural progenitor number is regulated by nuclear factor-kappaB p65 and p50 subunit-dependent proliferation rather than cell survival. Young, K.M., Bartlett, P.F., Coulson, E.J. J. Neurosci. Res. (2006) [Pubmed]
  5. Critical role for DP5/Harakiri, a Bcl-2 homology domain 3-only Bcl-2 family member, in axotomy-induced neuronal cell death. Imaizumi, K., Benito, A., Kiryu-Seo, S., Gonzalez, V., Inohara, N., Lieberman, A.P., Kiyama, H., Nuñez, G., Leiberman, A.P. J. Neurosci. (2004) [Pubmed]
  6. Up-regulated expression of genes encoding Hrk and IL-3R beta subunit by TCDD in vivo and in vitro. Park, J.H., Lee, S.W. Toxicol. Lett. (2002) [Pubmed]
 
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