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Gene Review

Ark  -  Apaf-1-related-killer

Drosophila melanogaster

Synonyms: APAF-1, APAF1, ARK, Apaf-1, Apaf1, ...
 
 
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Disease relevance of Ark

  • These mutants present a range of defects, including extensive hyperplasia of hematopoietic tissues, supernumerary neuronal cells, and head involution failure. dronc genetically interacts with the Ced4/Apaf1 counterpart, Dark, and adult structures lacking dronc are disrupted for fine patterning [1].
 

High impact information on Ark

  • Mutations affecting the Dark protein, an activator of the upstream caspase Dronc, also rescued RacN17 migration defects [2].
  • Control of the cell death pathway by Dapaf-1, a Drosophila Apaf-1/CED-4-related caspase activator [3].
  • Furthermore, orthologues of the apoptosome components, Ark (Apaf-1) and Dronc (caspase-9), are also required for the proper removal of bulk cytoplasm during spermatogenesis [4].
  • Inhibition of the Drosophila CED-4/Apaf-1-related killer (ARK) homologue resulted in pronounced inhibition of stress-induced apoptosis, whereas loss of ARK did not protect the cells from Reaper- or Grim-induced cell death [5].
  • In mammals and Drosophila, apoptotic caspases are under positive control via the CED-4/Apaf-1/Dark adaptors and negative control via IAPs (inhibitor of apoptosis proteins) [6].
 

Biological context of Ark

  • Dapaf-1 activities were also involved in cell death induced by ectopic expression of reaper in the compound eye [3].
  • Loss of Dapaf-1 function resulted in defective cytochrome c-dependent caspase activities and reduced apoptosis in embryo and in larval brain [3].
 

Associations of Ark with chemical compounds

 

Regulatory relationships of Ark

 

Other interactions of Ark

References

  1. The apical caspase dronc governs programmed and unprogrammed cell death in Drosophila. Chew, S.K., Akdemir, F., Chen, P., Lu, W.J., Mills, K., Daish, T., Kumar, S., Rodriguez, A., Abrams, J.M. Dev. Cell (2004) [Pubmed]
  2. A role for Drosophila IAP1-mediated caspase inhibition in Rac-dependent cell migration. Geisbrecht, E.R., Montell, D.J. Cell (2004) [Pubmed]
  3. Control of the cell death pathway by Dapaf-1, a Drosophila Apaf-1/CED-4-related caspase activator. Kanuka, H., Sawamoto, K., Inohara, N., Matsuno, K., Okano, H., Miura, M. Mol. Cell (1999) [Pubmed]
  4. The two Drosophila cytochrome C proteins can function in both respiration and caspase activation. Arama, E., Bader, M., Srivastava, M., Bergmann, A., Steller, H. EMBO J. (2006) [Pubmed]
  5. The role of ARK in stress-induced apoptosis in Drosophila cells. Zimmermann, K.C., Ricci, J.E., Droin, N.M., Green, D.R. J. Cell Biol. (2002) [Pubmed]
  6. Unrestrained caspase-dependent cell death caused by loss of Diap1 function requires the Drosophila Apaf-1 homolog, Dark. Rodriguez, A., Chen, P., Oliver, H., Abrams, J.M. EMBO J. (2002) [Pubmed]
  7. Inactivation of Drosophila Apaf-1 related killer suppresses formation of polyglutamine aggregates and blocks polyglutamine pathogenesis. Sang, T.K., Li, C., Liu, W., Rodriguez, A., Abrams, J.M., Zipursky, S.L., Jackson, G.R. Hum. Mol. Genet. (2005) [Pubmed]
  8. Three-dimensional structure of a double apoptosome formed by the Drosophila Apaf-1 related killer. Yu, X., Wang, L., Acehan, D., Wang, X., Akey, C.W. J. Mol. Biol. (2006) [Pubmed]
  9. Down-regulation of DIAP1 triggers a novel Drosophila cell death pathway mediated by Dark and DRONC. Igaki, T., Yamamoto-Goto, Y., Tokushige, N., Kanda, H., Miura, M. J. Biol. Chem. (2002) [Pubmed]
 
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