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Gene Review

Bid  -  BH3 interacting domain death agonist

Mus musculus

Synonyms: 2700049M22Rik, AI875481, AU022477, BH3-interacting domain death agonist, BID, ...
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Disease relevance of Bid

  • The volume of brain infarct is greatly reduced in Bid-deficient mice, thus indicating activation of the mitochondrial pathway by cell-death receptors following focal ischemia [1].
  • In contrast, loss of Bid, another BH3-only protein, provided no protection from neonatal HI brain injury [2].
  • Sustained phosphorylation of Bid is a marker for resistance to Fas-induced apoptosis during chronic liver diseases [3].
  • In controls, activation of the Fas receptor resulted in rapid dephosphorylation of Bid and its subsequent cleavage, whereas Bid remained phosphorylated and uncleaved in chronic cholestasis and other models of hepatic apoptosis resistance [3].
  • Oxygen deprivation of human colon cancer cells in vitro provoked decreased mRNA and protein levels of proapoptotic Bid and Bad [4].

High impact information on Bid


Chemical compound and disease context of Bid


Biological context of Bid


Anatomical context of Bid


Associations of Bid with chemical compounds


Physical interactions of Bid

  • Furthermore, it does not require Bid to interact directly with other Bcl-2 family proteins, such as Bax [12].
  • In vitro assays, using purified mitochondria and recombinant proteins, demonstrate that Bfl-1 binds full-length Bid, but does not interfere with its processing by caspase-8, or with its mitochondrial association [20].

Enzymatic interactions of Bid

  • In addition, caspase-8 cleaves Bid, the truncated form of which has the capacity to translocate to the mitochondria and induce cytochrome c release [1].
  • Moreover, in the absence of the putative transmembrane C-terminal domain, Bax does not form ionic channels in the presence of cut Bid [21].

Regulatory relationships of Bid

  • We discovered that Bid--a pro-death Bcl-2 family protein activated by ligated death receptors--was the main intracellular molecule signaling the generation of the radicals by targeting to the mitochondria and that the majority of oxygen radical production was dependent on Bid [22].
  • Among proapoptotic proteins, Bax expression was activated in H(2)S-treated cells but not Bid, and the antiapoptotic proteins Bcl-X(L) and Bcl-2 did not show any activation in pancreatic acinar cell apoptosis [23].
  • Furthermore, caspase-8 was activated and Bid cleaved [24].
  • The expression of Bcl-X(L) protected MLEC against H/R-induced cell death by blocking Bax and Bid translocation and inhibiting mitochondrial cytochrome c release [25].
  • Heat shock protein 90 suppresses tumor necrosis factor alpha induced apoptosis by preventing the cleavage of Bid in NIH3T3 fibroblasts [19].

Other interactions of Bid

  • The pro-death Bcl-2 family protein, Bid, mediates this pathway by inducing mitochondrial releases of cytochrome c and other apoptotic factors [14].
  • Among the Bcl-2 family proteins only Bid and Bcl-XL continue to be expressed at high levels in the adult brain [16].
  • We have, for the first time, identified a predominant role for the caspase-8/Bid pathway in signaling associated with hyperoxic lung injury and cell death in vivo and in vitro [11].
  • The expression of the pro-apoptotic members Bax, Bak, Bid, and Bcl-x(S) was significantly ( P < 0.05) decreased after TPN [26].
  • TNFR1/Fas engagement results in the cleavage of cytosolic Bid to truncated Bid (tBid), which translocates to mitochondria [27].

Analytical, diagnostic and therapeutic context of Bid


  1. Signaling of cell death and cell survival following focal cerebral ischemia: life and death struggle in the penumbra. Ferrer, I., Planas, A.M. J. Neuropathol. Exp. Neurol. (2003) [Pubmed]
  2. Selective involvement of BH3-only Bcl-2 family members Bim and Bad in neonatal hypoxia-ischemia. Ness, J.M., Harvey, C.A., Strasser, A., Bouillet, P., Klocke, B.J., Roth, K.A. Brain Res. (2006) [Pubmed]
  3. Sustained phosphorylation of Bid is a marker for resistance to Fas-induced apoptosis during chronic liver diseases. Vogel, A., Aslan, J.E., Willenbring, H., Klein, C., Finegold, M., Mount, H., Thomas, G., Grompe, M. Gastroenterology (2006) [Pubmed]
  4. Hypoxia-mediated down-regulation of Bid and Bax in tumors occurs via hypoxia-inducible factor 1-dependent and -independent mechanisms and contributes to drug resistance. Erler, J.T., Cawthorne, C.J., Williams, K.J., Koritzinsky, M., Wouters, B.G., Wilson, C., Miller, C., Demonacos, C., Stratford, I.J., Dive, C. Mol. Cell. Biol. (2004) [Pubmed]
  5. A role for proapoptotic BID in the DNA-damage response. Zinkel, S.S., Hurov, K.E., Ong, C., Abtahi, F.M., Gross, A., Korsmeyer, S.J. Cell (2005) [Pubmed]
  6. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. Luo, X., Budihardjo, I., Zou, H., Slaughter, C., Wang, X. Cell (1998) [Pubmed]
  7. Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis. Yin, X.M., Wang, K., Gross, A., Zhao, Y., Zinkel, S., Klocke, B., Roth, K.A., Korsmeyer, S.J. Nature (1999) [Pubmed]
  8. Bid deficiency ameliorates ischemic renal failure and delays animal death in C57BL/6 mice. Wei, Q., Yin, X.M., Wang, M.H., Dong, Z. Am. J. Physiol. Renal Physiol. (2006) [Pubmed]
  9. Proapoptotic Bid is required for pulmonary fibrosis. Budinger, G.R., Mutlu, G.M., Eisenbart, J., Fuller, A.C., Bellmeyer, A.A., Baker, C.M., Wilson, M., Ridge, K., Barrett, T.A., Lee, V.Y., Chandel, N.S. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  10. Nonredundant role of Bax and Bak in Bid-mediated apoptosis. Cartron, P.F., Juin, P., Oliver, L., Martin, S., Meflah, K., Vallette, F.M. Mol. Cell. Biol. (2003) [Pubmed]
  11. Necrotic cell death in response to oxidant stress involves the activation of the apoptogenic caspase-8/bid pathway. Wang, X., Ryter, S.W., Dai, C., Tang, Z.L., Watkins, S.C., Yin, X.M., Song, R., Choi, A.M. J. Biol. Chem. (2003) [Pubmed]
  12. Translocation of full-length Bid to mitochondria during anoikis. Valentijn, A.J., Gilmore, A.P. J. Biol. Chem. (2004) [Pubmed]
  13. Requirement for aspartate-cleaved bid in apoptosis signaling by DNA-damaging anti-cancer regimens. Werner, A.B., Tait, S.W., de Vries, E., Eldering, E., Borst, J. J. Biol. Chem. (2004) [Pubmed]
  14. Bid activates multiple mitochondrial apoptotic mechanisms in primary hepatocytes after death receptor engagement. Zhao, Y., Ding, W.X., Qian, T., Watkins, S., Lemasters, J.J., Yin, X.M. Gastroenterology (2003) [Pubmed]
  15. Bid is upstream of lysosome-mediated caspase 2 activation in tumor necrosis factor alpha-induced hepatocyte apoptosis. Guicciardi, M.E., Bronk, S.F., Werneburg, N.W., Yin, X.M., Gores, G.J. Gastroenterology (2005) [Pubmed]
  16. Dynamics of expression of apoptosis-regulatory proteins Bid, Bcl-2, Bcl-X, Bax and Bak during development of murine nervous system. Krajewska, M., Mai, J.K., Zapata, J.M., Ashwell, K.W., Schendel, S.L., Reed, J.C., Krajewski, S. Cell Death Differ. (2002) [Pubmed]
  17. Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injury. Zhao, Y., Li, S., Childs, E.E., Kuharsky, D.K., Yin, X.M. J. Biol. Chem. (2001) [Pubmed]
  18. Resistance of pancreatic cancer to gemcitabine treatment is dependent on mitochondria-mediated apoptosis. Schniewind, B., Christgen, M., Kurdow, R., Haye, S., Kremer, B., Kalthoff, H., Ungefroren, H. Int. J. Cancer (2004) [Pubmed]
  19. Heat shock protein 90 suppresses tumor necrosis factor alpha induced apoptosis by preventing the cleavage of Bid in NIH3T3 fibroblasts. Zhao, C., Wang, E. Cell. Signal. (2004) [Pubmed]
  20. Bcl-2 family member Bfl-1/A1 sequesters truncated bid to inhibit is collaboration with pro-apoptotic Bak or Bax. Werner, A.B., de Vries, E., Tait, S.W., Bontjer, I., Borst, J. J. Biol. Chem. (2002) [Pubmed]
  21. Bid induces cytochrome c-impermeable Bax channels in liposomes. Roucou, X., Rostovtseva, T., Montessuit, S., Martinou, J.C., Antonsson, B. Biochem. J. (2002) [Pubmed]
  22. Bid-dependent generation of oxygen radicals promotes death receptor activation-induced apoptosis in murine hepatocytes. Ding, W.X., Ni, H.M., DiFrancesca, D., Stolz, D.B., Yin, X.M. Hepatology (2004) [Pubmed]
  23. Mechanism of induction of pancreatic acinar cell apoptosis by hydrogen sulfide. Cao, Y., Adhikari, S., Ang, A.D., Moore, P.K., Bhatia, M. Am. J. Physiol., Cell Physiol. (2006) [Pubmed]
  24. Polycyclic aromatic hydrocarbons induce both apoptotic and anti-apoptotic signals in Hepa1c1c7 cells. Solhaug, A., Refsnes, M., Låg, M., Schwarze, P.E., Husøy, T., Holme, J.A. Carcinogenesis (2004) [Pubmed]
  25. Bcl-XL disrupts death-inducing signal complex formation in plasma membrane induced by hypoxia/reoxygenation. Wang, X., Zhang, J., Kim, H.P., Wang, Y., Choi, A.M., Ryter, S.W. FASEB J. (2004) [Pubmed]
  26. Total parenteral nutrition-induced apoptosis in mouse intestinal epithelium: regulation by the Bcl-2 protein family. Wildhaber, B.E., Lynn, K.N., Yang, H., Teitelbaum, D.H. Pediatr. Surg. Int. (2002) [Pubmed]
  27. tBid interaction with cardiolipin primarily orchestrates mitochondrial dysfunctions and subsequently activates Bax and Bak. Gonzalvez, F., Pariselli, F., Dupaigne, P., Budihardjo, I., Lutter, M., Antonsson, B., Diolez, P., Manon, S., Martinou, J.C., Goubern, M., Wang, X., Bernard, S., Petit, P.X. Cell Death Differ. (2005) [Pubmed]
  28. Bid-induced cytochrome c release is mediated by a pathway independent of mitochondrial permeability transition pore and Bax. Kim, T.H., Zhao, Y., Barber, M.J., Kuharsky, D.K., Yin, X.M. J. Biol. Chem. (2000) [Pubmed]
  29. Bid-mediated mitochondrial pathway is critical to ischemic neuronal apoptosis and focal cerebral ischemia. Yin, X.M., Luo, Y., Cao, G., Bai, L., Pei, W., Kuharsky, D.K., Chen, J. J. Biol. Chem. (2002) [Pubmed]
  30. Bid antisense attenuates bile acid-induced apoptosis and cholestatic liver injury. Higuchi, H., Miyoshi, H., Bronk, S.F., Zhang, H., Dean, N., Gores, G.J. J. Pharmacol. Exp. Ther. (2001) [Pubmed]
  31. Mechanism of hepatocytes apoptosis induced by the proapoptosis protein Bid. Bai, L., Cao, C.P., Mao, G.P. Chinese journal of digestive diseases. (2004) [Pubmed]
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