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Gene Review

Aifm1  -  apoptosis-inducing factor, mitochondrion...

Rattus norvegicus

Synonyms: Aif, Apoptosis-inducing factor 1, mitochondrial, Pdcd8, Programmed cell death protein 8
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Disease relevance of Pdcd8

  • Further, the nuclear translocation of AIF after ischemia was not blocked by inhibiting caspase-3/-7 activities, but, as shown in neuronal cultures that were challenged with transient oxygen-glucose deprivation, it can be prevented by intracellular delivery of the mitochondria-associated antiapoptotic protein Bcl-xL [1].
  • Translocation of apoptosis-inducing factor in vulnerable neurons after transient cerebral ischemia and in neuronal cultures after oxygen-glucose deprivation [1].
  • Here we report for the first time involvement of AIF in neuronal death induced by cerebral ischemia [2].
  • In the present study, we examined the role of AIF in ischemia-reperfusion injury in isolated rat hearts [3].
  • Intranuclear localization of AIF and large-scale DNA fragmentation occurs after TBI and in neurons under conditions of oxidative/nitrosative stress, providing the first evidence of this alternative mechanism by which programmed cell death may proceed in neurons after brain injury [4].

High impact information on Pdcd8


Chemical compound and disease context of Pdcd8


Biological context of Pdcd8


Anatomical context of Pdcd8


Associations of Pdcd8 with chemical compounds

  • When rats were treated with neuroprotective doses of cyclosporin A, but not with FK 506, the redistribution of apoptosis-inducing factor and cytochrome c was reduced and fodrin breakdown products and active caspase-3 immuno-reactivity was diminished whereas the extracellular calcium concentration was unaffected [10].
  • Neuron-enriched cultures exposed to peroxynitrite also demonstrated intranuclear AIF and large-scale DNA fragmentation concurrent with impaired mitochondrial respiration and cell death, events that are inhibited by treatment with a peroxynitrite decomposition catalyst [4].
  • The synergistic effects of an apoptosis-inducing factor, for example, the Arg-Gly-Asp (RGD) motif, can increase the radiotherapeutic efficacy of these peptides [16].
  • Using Hoechst 33342 or MTT assay, 10 muM Cd(2+) induced approximately 5-10% apoptosis in PT cells at 6 and 24 h, which was associated with cytochrome c and apoptosis-inducing factor release at 24 h only [17].
  • To study the mechanisms downstream from mitochondria that may cause neuronal death, we investigated the effects of cyclosporin A on subcellular localization of apoptosis-inducing factor and cytochrome c, activation of the cysteine proteases calpain and caspase-3, as well as its effect on brain extracellular calcium concentrations [10].

Other interactions of Pdcd8


Analytical, diagnostic and therapeutic context of Pdcd8


  1. Translocation of apoptosis-inducing factor in vulnerable neurons after transient cerebral ischemia and in neuronal cultures after oxygen-glucose deprivation. Cao, G., Clark, R.S., Pei, W., Yin, W., Zhang, F., Sun, F.Y., Graham, S.H., Chen, J. J. Cereb. Blood Flow Metab. (2003) [Pubmed]
  2. Involvement of apoptosis-inducing factor in neuronal death after hypoxia-ischemia in the neonatal rat brain. Zhu, C., Qiu, L., Wang, X., Hallin, U., Candé, C., Kroemer, G., Hagberg, H., Blomgren, K. J. Neurochem. (2003) [Pubmed]
  3. Role of apoptosis-inducing factor in myocardial cell death by ischemia-reperfusion. Kim, G.T., Chun, Y.S., Park, J.W., Kim, M.S. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
  4. Intranuclear localization of apoptosis-inducing factor (AIF) and large scale DNA fragmentation after traumatic brain injury in rats and in neuronal cultures exposed to peroxynitrite. Zhang, X., Chen, J., Graham, S.H., Du, L., Kochanek, P.M., Draviam, R., Guo, F., Nathaniel, P.D., Szabó, C., Watkins, S.C., Clark, R.S. J. Neurochem. (2002) [Pubmed]
  5. GD3 ganglioside directly targets mitochondria in a bcl-2-controlled fashion. Rippo, M.R., Malisan, F., Ravagnan, L., Tomassini, B., Condo, I., Costantini, P., Susin, S.A., Rufini, A., Todaro, M., Kroemer, G., Testi, R. FASEB J. (2000) [Pubmed]
  6. Innate gender-based proclivity in response to cytotoxicity and programmed cell death pathway. Du, L., Bayir, H., Lai, Y., Zhang, X., Kochanek, P.M., Watkins, S.C., Graham, S.H., Clark, R.S. J. Biol. Chem. (2004) [Pubmed]
  7. Epidermal growth factor triggers an original, caspase-independent pituitary cell death with heterogeneous phenotype. Fombonne, J., Reix, S., Rasolonjanahary, R., Danty, E., Thirion, S., Laforge-Anglade, G., Bosler, O., Mehlen, P., Enjalbert, A., Krantic, S. Mol. Biol. Cell (2004) [Pubmed]
  8. Cholesterol impairs the adenine nucleotide translocator-mediated mitochondrial permeability transition through altered membrane fluidity. Colell, A., García-Ruiz, C., Lluis, J.M., Coll, O., Mari, M., Fernández-Checa, J.C. J. Biol. Chem. (2003) [Pubmed]
  9. Intra-mitochondrial poly(ADP-ribosylation) contributes to NAD+ depletion and cell death induced by oxidative stress. Du, L., Zhang, X., Han, Y.Y., Burke, N.A., Kochanek, P.M., Watkins, S.C., Graham, S.H., Carcillo, J.A., Szabó, C., Clark, R.S. J. Biol. Chem. (2003) [Pubmed]
  10. Cyclosporin A prevents calpain activation despite increased intracellular calcium concentrations, as well as translocation of apoptosis-inducing factor, cytochrome c and caspase-3 activation in neurons exposed to transient hypoglycemia. Ferrand-Drake, M., Zhu, C., Gidö, G., Hansen, A.J., Karlsson, J.O., Bahr, B.A., Zamzami, N., Kroemer, G., Chan, P.H., Wieloch, T., Blomgren, K. J. Neurochem. (2003) [Pubmed]
  11. Translocation of AIF in the human and rat striatum following protracted haloperidol, but not clozapine treatment. Skoblenick, K.J., Castellano, J.M., Rogoza, R.M., Dyck, B.A., Thomas, N., Gabriele, J.P., Chong, V.Z., Mishra, R.K. Apoptosis (2006) [Pubmed]
  12. Glutamate-induced apoptosis in neuronal cells is mediated via caspase-dependent and independent mechanisms involving calpain and caspase-3 proteases as well as apoptosis inducing factor (AIF) and this process is inhibited by equine estrogens. Zhang, Y., Bhavnani, B.R. BMC neuroscience [electronic resource]. (2006) [Pubmed]
  13. Translocation of apoptosis-inducing factor in cerebellar granule cells exposed to neurotoxic agents inducing oxidative stress. Fonfría, E., Daré, E., Benelli, M., Suñol, C., Ceccatelli, S. Eur. J. Neurosci. (2002) [Pubmed]
  14. Nitric oxide-induced cell death in developing oligodendrocytes is associated with mitochondrial dysfunction and apoptosis-inducing factor translocation. Baud, O., Li, J., Zhang, Y., Neve, R.L., Volpe, J.J., Rosenberg, P.A. Eur. J. Neurosci. (2004) [Pubmed]
  15. Aging and lifelong calorie restriction result in adaptations of skeletal muscle apoptosis repressor, apoptosis-inducing factor, X-linked inhibitor of apoptosis, caspase-3, and caspase-12. Dirks, A.J., Leeuwenburgh, C. Free Radic. Biol. Med. (2004) [Pubmed]
  16. Increased cell death after therapy with an Arg-Gly-Asp-linked somatostatin analog. Capello, A., Krenning, E.P., Bernard, B.F., Breeman, W.A., van Hagen, M.P., de Jong, M. J. Nucl. Med. (2004) [Pubmed]
  17. Cd(2+)-induced cytochrome c release in apoptotic proximal tubule cells: role of mitochondrial permeability transition pore and Ca(2+) uniporter. Lee, W.K., Bork, U., Gholamrezaei, F., Thévenod, F. Am. J. Physiol. Renal Physiol. (2005) [Pubmed]
  18. Mitochondrial impairment induced by poly(ADP-ribose) polymerase-1 activation in cortical neurons after oxygen and glucose deprivation. Tanaka, S., Takehashi, M., Iida, S., Kitajima, T., Kamanaka, Y., Stedeford, T., Banasik, M., Ueda, K. J. Neurochem. (2005) [Pubmed]
  19. High molecular weight DNA fragments are processed by caspase sensitive or caspase independent pathways in cultures of cerebellar granule neurons. Slagsvold, H.H., Rosseland, C.M., Jacobs, C., Khuong, E., Kristoffersen, N., Gaarder, M., Fallgren, A.B., Huitfeldt, H.S., Paulsen, R.E. Brain Res. (2003) [Pubmed]
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