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Gene Review

Bid  -  BH3 interacting domain death agonist

Rattus norvegicus

Synonyms: BH3-interacting domain death agonist, BID, p22 BID
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Disease relevance of Bid

  • Temporal and spatial profile of Bid cleavage after experimental traumatic brain injury [1].
  • Consistently, Bid cleavage was also induced following ATP depletion by hypoxia or mitochondrial uncoupling [2].
  • Together, these results provide the first evidence for Bid activation in kidney cells following ATP depletion in vitro and renal ischemia in vivo [2].
  • Moreover, we have shown that unlike the pro-apoptotic protein Bid, the toxicity associated with the transient expression of Bcl-2 occurs independent of the activity of the endogenous Bax [3].
  • Calpain inhibitors prevented cleavage of Bid as well as the downstream indices of cell death, including DNA strand breaks, creatine kinase (CK) release, and infarction measured by triphenyl tetrazolium chloride (TTC) staining [4].

High impact information on Bid

  • Fas-associated death domain protein, procaspase-8, procaspase-10, c-Jun amino-terminal kinase, and Bid were recruited into rafts, linking Fas and mitochondrial signaling routes [5].
  • Bcl-xL can inhibit the effect of Bid by interacting directly with Bax [6].
  • Here we report that in staurosporine-induced apoptosis of HeLa cells, Bid, a BH3 domain containing protein, translocates from the cytosol to mitochondria [6].
  • Consistently, Bid/Bik induced apoptosis without Deltapsi loss, whereas Bax induced apoptosis with Deltapsi loss [7].
  • However, caspase activation mediates cleavage of Bid and Bcl-xL that could originate an amplification loop on the mitochondrial events [8].

Biological context of Bid


Anatomical context of Bid

  • The largely uninjured contralateral hippocampus did not exhibit Bid cleavage or binding of 14-3-3 to Bid [12].
  • Pelleting experiments with paclitaxel-stabilized microtubules show that Bak is associated with the microtubule pellet, whereas Bid remains primarily with the unpolymerized fraction [13].
  • The results provide the first evidence of Bid cleavage in the traumatized cortex after experimental traumatic brain injury in vivo, and demonstrate that tBid is expressed in neurons and glial cells [1].
  • Of significance, cleaved Bid translocated to mitochondria, suggesting a role for Bid in the development of mitochondrial defects in ATP-depleted cells [2].
  • The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol [14].

Associations of Bid with chemical compounds


Enzymatic interactions of Bid


Regulatory relationships of Bid


Other interactions of Bid

  • Exposure to C5b-9 induced an inhibition of caspase-8 activation, Bid cleavage, and a significant increase in expression of cellular FLIP long isoform [20].
  • Coimmunoprecipitation analysis demonstrated that although Bcl-2-associated death promoter (Bad) constitutively bound 14-3-3, there was no interaction between Bid and 14-3-3 in control brain [12].
  • Activation of caspase-8 and cleavage of Bid to tBid in RGC-5 cells following exposure to IFN-gamma indicated co-operation between extrinsic and intrinsic pathways of apoptosis [21].
  • In contrast, there was no evidence of caspase-8 or caspase-9 processing or Bid cleavage in the ipsilateral hippocampus, contralateral cortex, and hippocampus up to 7 days after the injury [1].
  • These results suggested that removal of N-terminal domains of Bid by caspase-8 and Mcl-1 by caspase-3 enabled the maximal mitochondrial perturbation that potentiated TRAIL-induced apoptosis [22].

Analytical, diagnostic and therapeutic context of Bid


  1. Temporal and spatial profile of Bid cleavage after experimental traumatic brain injury. Franz, G., Beer, R., Intemann, D., Krajewski, S., Reed, J.C., Engelhardt, K., Pike, B.R., Hayes, R.L., Wang, K.K., Schmutzhard, E., Kampfl, A. J. Cereb. Blood Flow Metab. (2002) [Pubmed]
  2. Bid activation in kidney cells following ATP depletion in vitro and ischemia in vivo. Wei, Q., Alam, M.M., Wang, M.H., Yu, F., Dong, Z. Am. J. Physiol. Renal Physiol. (2004) [Pubmed]
  3. Apoptosis modulatory activities of transiently expressed Bcl-2: roles in cytochrome C release and Bax regulation. Hou, Q., Cymbalyuk, E., Hsu, S.C., Xu, M., Hsu, Y.T. Apoptosis (2003) [Pubmed]
  4. Calpain and mitochondria in ischemia/reperfusion injury. Chen, M., Won, D.J., Krajewski, S., Gottlieb, R.A. J. Biol. Chem. (2002) [Pubmed]
  5. Intracellular triggering of Fas aggregation and recruitment of apoptotic molecules into Fas-enriched rafts in selective tumor cell apoptosis. Gajate, C., Del Canto-Jañez, E., Acuña, A.U., Amat-Guerri, F., Geijo, E., Santos-Beneit, A.M., Veldman, R.J., Mollinedo, F. J. Exp. Med. (2004) [Pubmed]
  6. Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis. Desagher, S., Osen-Sand, A., Nichols, A., Eskes, R., Montessuit, S., Lauper, S., Maundrell, K., Antonsson, B., Martinou, J.C. J. Cell Biol. (1999) [Pubmed]
  7. Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity. Shimizu, S., Tsujimoto, Y. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  8. Activation of caspases occurs downstream from radical oxygen species production, Bcl-xL down-regulation, and early cytochrome C release in apoptosis induced by transforming growth factor beta in rat fetal hepatocytes. Herrera, B., Fernández, M., Alvarez, A.M., Roncero, C., Benito, M., Gil, J., Fabregat, I. Hepatology (2001) [Pubmed]
  9. Inhibition of caspase-8 attenuates neuronal death induced by limbic seizures in a cytochrome c-dependent and Smac/DIABLO-independent way. Li, T., Lu, C., Xia, Z., Xiao, B., Luo, Y. Brain Res. (2006) [Pubmed]
  10. Real time single cell analysis of Bid cleavage and Bid translocation during caspase-dependent and neuronal caspase-independent apoptosis. Ward, M.W., Rehm, M., Duessmann, H., Kacmar, S., Concannon, C.G., Prehn, J.H. J. Biol. Chem. (2006) [Pubmed]
  11. JNK mediates hepatic ischemia reperfusion injury. Uehara, T., Bennett, B., Sakata, S.T., Satoh, Y., Bilter, G.K., Westwick, J.K., Brenner, D.A. J. Hepatol. (2005) [Pubmed]
  12. Interaction of 14-3-3 with Bid during seizure-induced neuronal death. Shinoda, S., Schindler, C.K., Quan-Lan, J., Saugstad, J.A., Taki, W., Simon, R.P., Henshall, D.C. J. Neurochem. (2003) [Pubmed]
  13. Direct interaction of Bcl-2 proteins with tubulin. Knipling, L., Wolff, J. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  14. The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol. Kluck, R.M., Esposti, M.D., Perkins, G., Renken, C., Kuwana, T., Bossy-Wetzel, E., Goldberg, M., Allen, T., Barber, M.J., Green, D.R., Newmeyer, D.D. J. Cell Biol. (1999) [Pubmed]
  15. Minocycline up-regulates Bcl-2 and protects against cell death in mitochondria. Wang, J., Wei, Q., Wang, C.Y., Hill, W.D., Hess, D.C., Dong, Z. J. Biol. Chem. (2004) [Pubmed]
  16. Bid acts on the permeability transition pore complex to induce apoptosis. Zamzami, N., El Hamel, C., Maisse, C., Brenner, C., Muñoz-Pinedo, C., Belzacq, A.S., Costantini, P., Vieira, H., Loeffler, M., Molle, G., Kroemer, G. Oncogene (2000) [Pubmed]
  17. Bleomycin induces alveolar epithelial cell death through JNK-dependent activation of the mitochondrial death pathway. Lee, V.Y., Schroedl, C., Brunelle, J.K., Buccellato, L.J., Akinci, O.I., Kaneto, H., Snyder, C., Eisenbart, J., Budinger, G.R., Chandel, N.S. Am. J. Physiol. Lung Cell Mol. Physiol. (2005) [Pubmed]
  18. Minimal BH3 peptides promote cell death by antagonizing anti-apoptotic proteins. Moreau, C., Cartron, P.F., Hunt, A., Meflah, K., Green, D.R., Evan, G., Vallette, F.M., Juin, P. J. Biol. Chem. (2003) [Pubmed]
  19. Apoptosis-inducing factor triggered by poly(ADP-ribose) polymerase and Bid mediates neuronal cell death after oxygen-glucose deprivation and focal cerebral ischemia. Culmsee, C., Zhu, C., Landshamer, S., Becattini, B., Wagner, E., Pellecchia, M., Pellechia, M., Blomgren, K., Plesnila, N. J. Neurosci. (2005) [Pubmed]
  20. C5b-9 terminal complex protects oligodendrocytes from apoptotic cell death by inhibiting caspase-8 processing and up-regulating FLIP. Cudrici, C., Niculescu, F., Jensen, T., Zafranskaia, E., Fosbrink, M., Rus, V., Shin, M.L., Rus, H. J. Immunol. (2006) [Pubmed]
  21. Calpeptin provides functional neuroprotection to rat retinal ganglion cells following Ca2+ influx. Das, A., Garner, D.P., Del Re, A.M., Woodward, J.J., Kumar, D.M., Agarwal, N., Banik, N.L., Ray, S.K. Brain Res. (2006) [Pubmed]
  22. Specific cleavage of Mcl-1 by caspase-3 in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in Jurkat leukemia T cells. Weng, C., Li, Y., Xu, D., Shi, Y., Tang, H. J. Biol. Chem. (2005) [Pubmed]
  23. The heterocyclic amine, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole induces apoptosis in cocultures of rat parenchymal and nonparenchymal liver cells. Ashida, H., Kihara, K., Nonaka, Y., Fukuda, I., Shiotani, B., Hashimoto, T. Toxicol. Appl. Pharmacol. (2001) [Pubmed]
  24. Cytochrome c release into cytosol with subsequent caspase activation during warm ischemia in rat liver. Soeda, J., Miyagawa, S., Sano, K., Masumoto, J., Taniguchi, S., Kawasaki, S. Am. J. Physiol. Gastrointest. Liver Physiol. (2001) [Pubmed]
  25. Mitochondrial-dependent apoptosis in experimental rodent abdominal aortic aneurysms. Sinha, I., Sinha-Hikim, A.P., Hannawa, K.K., Henke, P.K., Eagleton, M.J., Stanley, J.C., Upchurch, G.R. Surgery (2005) [Pubmed]
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