Bax

Summary

Gene Symbol: Bax
Description: BCL2 associated X, apoptosis regulator
Alias: apoptosis regulator BAX, Bcl2-associated X protein
Species: rat
Products:     Bax

Top Publications

  1. Jin K, Graham S, Mao X, He X, Nagayama T, Simon R, et al. Bax kappa, a novel Bax splice variant from ischemic rat brain lacking an ART domain, promotes neuronal cell death. J Neurochem. 2001;77:1508-19 pubmed
    b>Bax is a pro-apoptotic Bcl-2 family protein that regulates programmed cell death through homodimerization and through heterodimerization with Bcl-2. Bax alpha is encoded by six exons and undergoes alternative splicing...
  2. Jafari Anarkooli I, Sankian M, Ahmadpour S, Varasteh A, Haghir H. Evaluation of Bcl-2 family gene expression and Caspase-3 activity in hippocampus STZ-induced diabetic rats. Exp Diabetes Res. 2008;2008:638467 pubmed publisher
    ..The expressions of Bcl-2, Bcl-x(L), and Bax mRNA and proteins were measured using RT-PCR and western blotting, respectively...
  3. Qiao W, Wang G, Shi Y, Wu J, Qi Y, Zhang J, et al. Differential expression of Bcl-2 and Bax during gastric ischemia-reperfusion of rats. World J Gastroenterol. 2011;17:1718-24 pubmed publisher
    To investigate expression of Bcl-2 and Bax in gastric ischemia-reperfusion (GI-R) and involvement of extracellular signal-regulated kinase (ERK) 1/2 activation...
  4. Deckwerth T, Elliott J, Knudson C, Johnson E, Snider W, Korsmeyer S. BAX is required for neuronal death after trophic factor deprivation and during development. Neuron. 1996;17:401-11 pubmed
    Members of the BCL2-related family of proteins either promote or repress programmed cell death. BAX, a death-promoting member, heterodimerizes with multiple death-repressing molecules, suggesting that it could prove critical to cell ..
  5. Karbowski M, Norris K, Cleland M, Jeong S, Youle R. Role of Bax and Bak in mitochondrial morphogenesis. Nature. 2006;443:658-62 pubmed
    ..Two members of the Bcl-2 family, Bax and Bak, change intracellular location early in the promotion of apoptosis to concentrate in focal clusters at ..
  6. Antonsson B, Conti F, Ciavatta A, Montessuit S, Lewis S, Martinou I, et al. Inhibition of Bax channel-forming activity by Bcl-2. Science. 1997;277:370-2 pubmed
    ..b>Bax, a pro-apoptotic member of the Bcl-2 family, was shown to form channels in lipid membranes...
  7. Tan C, Dlugosz P, Peng J, Zhang Z, Lapolla S, Plafker S, et al. Auto-activation of the apoptosis protein Bax increases mitochondrial membrane permeability and is inhibited by Bcl-2. J Biol Chem. 2006;281:14764-75 pubmed
    ..The interactions between BH3 region-only proteins and multi-BH region proteins such as Bax and Bcl-2 have been proposed to be the dominant interactions required for initiating apoptosis...
  8. Takahashi Y, Karbowski M, Yamaguchi H, Kazi A, Wu J, Sebti S, et al. Loss of Bif-1 suppresses Bax/Bak conformational change and mitochondrial apoptosis. Mol Cell Biol. 2005;25:9369-82 pubmed
    Bif-1, a member of the endophilin B protein family, interacts with Bax and promotes interleukin-3 withdrawal-induced Bax conformational change and apoptosis when overexpressed in FL5.12 cells...
  9. Capano M, Crompton M. Biphasic translocation of Bax to mitochondria. Biochem J. 2002;367:169-78 pubmed
    Using green fluorescent protein-tagged Bax, we demonstrate that Bax is sequestered from the cytosol of cardiomyocytes in two distinct phases following the induction of apoptosis with staurosporine...

More Information

Publications62

  1. Mosinger Ogilvie J, Deckwerth T, Knudson C, Korsmeyer S. Suppression of developmental retinal cell death but not of photoreceptor degeneration in Bax-deficient mice. Invest Ophthalmol Vis Sci. 1998;39:1713-20 pubmed
    b>Bax, a member of the Bcl2 family of cell death regulators, induces cell death by promoting the induction of apoptosis...
  2. Yang E, Zha J, Jockel J, Boise L, Thompson C, Korsmeyer S. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell. 1995;80:285-91 pubmed
    ..Bad selectively dimerized with Bcl-xL as well as Bcl-2, but not with Bax, Bcl-xs, Mcl-1, A1, or itself...
  3. Harris C, Johnson E. BH3-only Bcl-2 family members are coordinately regulated by the JNK pathway and require Bax to induce apoptosis in neurons. J Biol Chem. 2001;276:37754-60 pubmed
    ..Here we show that the BH3-only Bcl-2 family members, Dp5/Hrk and Bim, are induced upstream of the Bax checkpoint in neuronal apoptosis in a manner that shows significant dependence on JNK signaling...
  4. Cregan S, MacLaurin J, Craig C, Robertson G, Nicholson D, Park D, et al. Bax-dependent caspase-3 activation is a key determinant in p53-induced apoptosis in neurons. J Neurosci. 1999;19:7860-9 pubmed
    ..To determine whether Bax is essential for caspase-3 activation, p53 was expressed in Bax-deficient cells...
  5. Narita M, Shimizu S, Ito T, Chittenden T, Lutz R, Matsuda H, et al. Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria. Proc Natl Acad Sci U S A. 1998;95:14681-6 pubmed
    ..Using isolated mitochondria, we found that recombinant Bax and Bak, proapoptotic members of the Bcl-2 family, induced mitochondrial Deltapsi loss, swelling, and cytochrome c ..
  6. Shibue T, Takeda K, Oda E, Tanaka H, Murasawa H, Takaoka A, et al. Integral role of Noxa in p53-mediated apoptotic response. Genes Dev. 2003;17:2233-8 pubmed
    ..apoptosis in response to DNA damage, which was further increased by introducing an additional null zygosity for Bax. These MEFs also showed increased sensitivity to oncogene-induced cell transformation in vitro...
  7. Dong H, Fazzaro A, Xiang C, Korsmeyer S, Jacquin M, McDonald J. Enhanced oligodendrocyte survival after spinal cord injury in Bax-deficient mice and mice with delayed Wallerian degeneration. J Neurosci. 2003;23:8682-91 pubmed
    ..death after spinal cord injury (SCI) were evaluated by T9 cord level hemisection in wild-type mice (C57BL/6J and Bax+/+ mice), Wlds mice in which severed axons remain viable for 2 weeks, and mice deficient in the proapoptotic ..
  8. Karbowski M, Lee Y, Gaume B, Jeong S, Frank S, Nechushtan A, et al. Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis. J Cell Biol. 2002;159:931-8 pubmed
    We find that Bax, a proapoptotic member of the Bcl-2 family, translocates to discrete foci on mitochondria during the initial stages of apoptosis, which subsequently become mitochondrial scission sites...
  9. Hetz C, Bernasconi P, Fisher J, Lee A, Bassik M, Antonsson B, et al. Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alpha. Science. 2006;312:572-6 pubmed
    ..We investigated UPR signaling events in mice in the absence of the proapoptotic BCL-2 family members BAX and BAK [double knockout (DKO)]...
  10. Willis S, Chen L, Dewson G, Wei A, Naik E, Fletcher J, et al. Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. Genes Dev. 2005;19:1294-305 pubmed
    ..proteins trigger apoptosis by binding via their BH3 domain to prosurvival relatives, while the proapoptotic Bax and Bak have an essential downstream role involving permeabilization of organellar membranes and induction of ..
  11. Lindsten T, Ross A, King A, Zong W, Rathmell J, Shiels H, et al. The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues. Mol Cell. 2000;6:1389-99 pubmed
    ..However, mice lacking bax display limited phenotypic abnormalities...
  12. Antonsson B, Montessuit S, Lauper S, Eskes R, Martinou J. Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria. Biochem J. 2000;345 Pt 2:271-8 pubmed
    b>Bax is a Bcl-2-family protein with pro-apoptotic activity that can form channels in lipid membranes. The protein has been shown to trigger cytochrome c release from mitochondria both in vitro and in vivo...
  13. Vukosavic S, Dubois Dauphin M, Romero N, Przedborski S. Bax and Bcl-2 interaction in a transgenic mouse model of familial amyotrophic lateral sclerosis. J Neurochem. 1999;73:2460-8 pubmed
    ..In asymptomatic transgenic mSOD1 mice, expression of Bcl-2, Bcl-XL, Bad, and Bax does not differ from that in nontransgenic mice...
  14. Wang K, Yin X, Chao D, Milliman C, Korsmeyer S. BID: a novel BH3 domain-only death agonist. Genes Dev. 1996;10:2859-69 pubmed
    The BCL-2 family of proteins consists of both antagonists (e.g., BCL-2) and agonists (e.g., BAX) that regulate apoptosis and compete through dimerization...
  15. Coassin M, Lambiase A, Sposato V, Micera A, Bonini S, Aloe L. Retinal p75 and bax overexpression is associated with retinal ganglion cells apoptosis in a rat model of glaucoma. Graefes Arch Clin Exp Ophthalmol. 2008;246:1743-9 pubmed publisher
    ..Retinal ganglion cell (RGC) apoptosis, retinal expression of NGF protein as well as Bcl-2, Bax, trkA(NGFR) and p75(NTR) transcript expression were detected...
  16. Roucou X, Montessuit S, Antonsson B, Martinou J. Bax oligomerization in mitochondrial membranes requires tBid (caspase-8-cleaved Bid) and a mitochondrial protein. Biochem J. 2002;368:915-21 pubmed
    In response to various apoptotic stimuli, Bax, a pro-apoptotic member of the Bcl-2 family, is oligomerized and permeabilizes the mitochondrial outer membrane to apoptogenic factors, including cytochrome c...
  17. Chipuk J, Kuwana T, Bouchier Hayes L, Droin N, Newmeyer D, Schuler M, et al. Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis. Science. 2004;303:1010-4 pubmed
    ..p53 directly activated the proapoptotic Bcl-2 protein Bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program...
  18. Lakhani S, Masud A, Kuida K, Porter G, Booth C, Mehal W, et al. Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science. 2006;311:847-51 pubmed
    ..Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed...
  19. Knudson C, Korsmeyer S. Bcl-2 and Bax function independently to regulate cell death. Nat Genet. 1997;16:358-63 pubmed
    ..Using a genetic approach to address this question, we utilized gain- and loss-of-function models of Bcl-2 and Bax and found that apoptosis and thymic hypoplasia characteristic of Bcl-2-deficient mice are largely absent in mice ..
  20. Yethon J, Epand R, Leber B, Epand R, Andrews D. Interaction with a membrane surface triggers a reversible conformational change in Bax normally associated with induction of apoptosis. J Biol Chem. 2003;278:48935-41 pubmed
    The Bcl-2 family member Bax is an apoptosis-promoting protein that normally resides in an inactive state within the cytoplasm of healthy cells...
  21. Hsu Y, Youle R. Bax in murine thymus is a soluble monomeric protein that displays differential detergent-induced conformations. J Biol Chem. 1998;273:10777-83 pubmed
    Bcl-2, Bcl-XL, and Bax are members of the Bcl-2 family that play important roles in apoptosis regulation. These proteins are believed to be membrane-bound and to regulate apoptosis through formation of homo- and heterodimers...
  22. White F, Keller Peck C, Knudson C, Korsmeyer S, Snider W. Widespread elimination of naturally occurring neuronal death in Bax-deficient mice. J Neurosci. 1998;18:1428-39 pubmed
    The proapoptotic molecule BAX is required for death of sympathetic and motor neurons in the setting of trophic factor deprivation. Furthermore, adult Bax-/- mice have more motor neurons than do their wild-type counterparts...
  23. Gill M, Bockhorst K, Narayana P, Perez Polo J. Bax shuttling after neonatal hypoxia-ischemia: hyperoxia effects. J Neurosci Res. 2008;86:3584-604 pubmed publisher
    ..Here, we provide evidence that Bcl-2-associated X protein (Bax) can shuttle to different subcellular compartments in response to HI, thus triggering the different organelle-..
  24. Dlugosz P, Billen L, Annis M, Zhu W, Zhang Z, Lin J, et al. Bcl-2 changes conformation to inhibit Bax oligomerization. EMBO J. 2006;25:2287-96 pubmed
    ..Oligomerization of Bax promotes cell death by permeabilizing the outer mitochondrial membrane...
  25. Lovell J, Billen L, Bindner S, Shamas Din A, Fradin C, Leber B, et al. Membrane binding by tBid initiates an ordered series of events culminating in membrane permeabilization by Bax. Cell. 2008;135:1074-84 pubmed publisher
    ..However, the rules of engagement between the pro- and antiapoptotic family members are still contested, and how Bax is transformed from a cytosolic monomer to an outer mitochondrial membrane-permeabilizing oligomer is unclear...
  26. Sánchez Gómez M, Alberdi E, Pérez Navarro E, Alberch J, Matute C. Bax and calpain mediate excitotoxic oligodendrocyte death induced by activation of both AMPA and kainate receptors. J Neurosci. 2011;31:2996-3006 pubmed publisher
    ..Here, we provide evidence that Bax, a proapoptotic member of the Bcl-2 protein family, is involved in excitotoxic apoptotic death of oligodendrocytes ..
  27. Oltvai Z, Milliman C, Korsmeyer S. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell. 1993;74:609-19 pubmed
    ..We identified an associated 21 kd protein partner, Bax, that has extensive amino acid homology with Bcl-2, focused within highly conserved domains I and II...
  28. Lin C, Lu Y, Cheng F, Chu L, Hsueh C. Bax-regulated mitochondria-mediated apoptosis is responsible for the in vitro ischemia induced neuronal cell death of Sprague Dawley rat. Neurosci Lett. 2005;387:22-7 pubmed
    ..The death rate, degree of the apoptotic damage, reduction of mitochondrial membrane potential, translocation of Bax, release of cytochrome C and activation of caspase-9 and -3 were determined at each time point...
  29. Knudson C, Tung K, Tourtellotte W, Brown G, Korsmeyer S. Bax-deficient mice with lymphoid hyperplasia and male germ cell death. Science. 1995;270:96-9 pubmed
    b>BAX, a heterodimeric partner of BCL2, counters BCL2 and promotes apoptosis in gain-of-function experiments. A Bax knockout mouse was generated that proved viable but displayed lineage-specific aberrations in cell death...
  30. Cartron P, Arokium H, Oliver L, Meflah K, Manon S, Vallette F. Distinct domains control the addressing and the insertion of Bax into mitochondria. J Biol Chem. 2005;280:10587-98 pubmed
    The translocation of Bax from the cytosol into the mitochondrial outer membrane is a central event during apoptosis...
  31. Jurgensmeier J, Xie Z, Deveraux Q, Ellerby L, Bredesen D, Reed J. Bax directly induces release of cytochrome c from isolated mitochondria. Proc Natl Acad Sci U S A. 1998;95:4997-5002 pubmed
    b>Bax is a pro-apoptotic member of the Bcl-2 protein family that resides in the outer mitochondrial membrane...
  32. Zhao J, Wang L, Nie J, Niu Q. [Effects of benzo(a)pyrene on apoptosis of neuronal cells and expression of Bcl-2 and Bax proteins in rat brain tissue]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2011;29:820-4 pubmed
    To observe the effects of Benzo(a)pyrene (BaP) on apoptosis of neuronal cells and expression of Bcl-2 and Bax proteins and to explore the mechanism of neurotoxicity induced by BaP in rats...
  33. Kroeger H, Messah C, Ahern K, Gee J, Joseph V, Matthes M, et al. Induction of endoplasmic reticulum stress genes, BiP and chop, in genetic and environmental models of retinal degeneration. Invest Ophthalmol Vis Sci. 2012;53:7590-9 pubmed publisher
  34. Simonishvili S, Jain M, Li H, Levison S, Wood T. Identification of Bax-interacting proteins in oligodendrocyte progenitors during glutamate excitotoxicity and perinatal hypoxia-ischemia. ASN Neuro. 2013;5:e00131 pubmed publisher
    ..CNS disorders, and previous studies have demonstrated that AMPA/kainate receptors require the pro-apoptotic protein Bax in OPCs undergoing apoptosis...
  35. Park M, Joo S, Kim B, Lee J, Kim Y, Hong M, et al. Remote Preconditioning on Rat Hepatic Ischemia-Reperfusion Injury Downregulated Bax and Cleaved Caspase-3 Expression. Transplant Proc. 2016;48:1247-50 pubmed publisher
    ..For Bax/?-actin, mean values of the 3 groups (±standard deviation) were 1.29 ± 0.26 (group I), 0.89 ± 0...
  36. Wang Y, Ausman L, Russell R, Greenberg A, Wang X. Increased apoptosis in high-fat diet-induced nonalcoholic steatohepatitis in rats is associated with c-Jun NH2-terminal kinase activation and elevated proapoptotic Bax. J Nutr. 2008;138:1866-71 pubmed
    ..concentrations of cleaved caspase-3, cytochrome p4502E1 (CYP2E1), phosphorylated c-Jun NH(2)-terminal kinase (JNK), Bax, Bcl-2, and Bcl-xl were measured...
  37. Vila M, Jackson Lewis V, Vukosavic S, Djaldetti R, Liberatore G, Offen D, et al. Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. Proc Natl Acad Sci U S A. 2001;98:2837-42 pubmed
    ..Here, we show that the pro-apoptotic protein Bax is highly expressed in the SNpc and that its ablation attenuates SNpc developmental neuronal apoptosis...
  38. Siddiqui I, Shukla Y, Adhami V, Sarfaraz S, Asim M, Hafeez B, et al. Suppression of NFkappaB and its regulated gene products by oral administration of green tea polyphenols in an autochthonous mouse prostate cancer model. Pharm Res. 2008;25:2135-42 pubmed publisher
    ..Therefore, we analyzed Bax and Bcl2 levels in the dorsolateral prostate of TRAMP mice fed GTP and observed a shift in balance between Bax and ..
  39. Meijerink J, Mensink E, Wang K, Sedlak T, Sloetjes A, de Witte T, et al. Hematopoietic malignancies demonstrate loss-of-function mutations of BAX. Blood. 1998;91:2991-7 pubmed
    ..Recently, studies of Bax-deficient mice have indicated that the pro-apoptotic BAX molecule can function as a tumor suppressor...
  40. Tan K, Fu N, Sukumaran S, Chan S, Kang J, Poon K, et al. MAP-1 is a mitochondrial effector of Bax. Proc Natl Acad Sci U S A. 2005;102:14623-8 pubmed
    Apoptotic stimuli induce conformational changes in Bax and trigger its translocation from cytosol to mitochondria...
  41. Lang Rollin I, Maniati M, Jabado O, Vekrellis K, Papantonis S, Rideout H, et al. Apoptosis and the conformational change of Bax induced by proteasomal inhibition of PC12 cells are inhibited by bcl-xL and bcl-2. Apoptosis. 2005;10:809-20 pubmed
    ..Furthermore, Bax undergoes a conformational change and is translocated to the mitochondria in a caspase-independent fashion...
  42. Shimohama S, Fujimoto S, Sumida Y, Tanino H. Differential expression of rat brain bcl-2 family proteins in development and aging. Biochem Biophys Res Commun. 1998;252:92-6 pubmed
    ..previously examined the involvement of the B cell leukemia-2 gene product (Bcl-2) family proteins (Bcl-2, Bcl-x, Bax, Bak, and Bad) in Alzheimer's disease (AD) and found that Bcl-2, Bcl-x, Bak, and Bad were upregulated...
  43. Lee J, Takahashi T, Yasuhara N, Inazawa J, Kamada S, Tsujimoto Y. Bis, a Bcl-2-binding protein that synergizes with Bcl-2 in preventing cell death. Oncogene. 1999;18:6183-90 pubmed
    ..indicated that Bis itself exerted only weak anti-apoptotic activity, but was synergistic with Bcl-2 in preventing Bax-induced and Fas-mediated apoptosis...
  44. Suzuki H, Tsuda M, Kiso M, Saga Y. Nanos3 maintains the germ cell lineage in the mouse by suppressing both Bax-dependent and -independent apoptotic pathways. Dev Biol. 2008;318:133-42 pubmed publisher
    ..mouse embryo, Steel/c-Kit signaling is required to prevent migrating primordial germ cells (PGCs) from undergoing Bax-dependent apoptosis...
  45. Lu D, Sivaprasad U, Huang J, Shankar E, Morrow S, Basu A. Protein kinase C-epsilon protects MCF-7 cells from TNF-mediated cell death by inhibiting Bax translocation. Apoptosis. 2007;12:1893-900 pubmed
    ..Depletion of Bax by small interfering RNA (siRNA) attenuated TNF-induced cell death...
  46. Khor L, Moughan J, Al Saleem T, Hammond E, Venkatesan V, Rosenthal S, et al. Bcl-2 and Bax expression predict prostate cancer outcome in men treated with androgen deprivation and radiotherapy on radiation therapy oncology group protocol 92-02. Clin Cancer Res. 2007;13:3585-90 pubmed
    ..b>Bax is proapoptotic, regulating Bcl-2 through heterodimer formation...
  47. Vogt M, Butz K, Dymalla S, Semzow J, Hoppe Seyler F. Inhibition of Bax activity is crucial for the antiapoptotic function of the human papillomavirus E6 oncoprotein. Oncogene. 2006;25:4009-15 pubmed
    ..This is linked to the activation and translocation of Bax to the mitochondrial membrane, cytochrome c release into the cytosol, and activation of caspase-3, in a PUMA-..
  48. Bhattacharjee M, Acharya S, Ghosh A, Sarkar P, Chatterjee S, Kumar P, et al. Bax and Bid act in synergy to bring about T11TS-mediated glioma apoptosis via the release of mitochondrial cytochrome c and subsequent caspase activation. Int Immunol. 2008;20:1489-505 pubmed publisher
    ..The proteins that were selected could be divided into three broad classes-the Bcl-2 family of proteins-Bid, Bax and Bcl-2; the guardian of the genome p53 and the proteins downstream of mitochondria-Apaf-1, cytochrome c, caspase-..
  49. Levkovitch Verbin H, Makarovsky D, Vander S. Comparison between axonal and retinal ganglion cell gene expression in various optic nerve injuries including glaucoma. Mol Vis. 2013;19:2526-41 pubmed
    ..The proapoptotic genes, BCL2-associated X protein (BAX) and Bcl-2-associated death promoter (BAD), were significantly upregulated in both injured retinas and ONs...
  50. Lai X, Ye S, Zheng L, Li L, Liu Q, Yu S, et al. Selective 14-3-3? induction quenches p-?-catenin Ser37/Bax-enhanced cell death in cerebral cortical neurons during ischemia. Cell Death Dis. 2014;5:e1184 pubmed publisher
    ..a selective ischemia-inducible survival factor in cerebral cortical neurons reducing cell death by downregulating Bax depend direct 14-3-3?/p-?-catenin Ser37 interactions in the nucleus...
  51. Liang M, Li A, Lou A, Zhang X, Chen Y, Yang L, et al. Advanced oxidation protein products promote NADPH oxidase-dependent β-cell destruction and dysfunction through the Bcl-2/Bax apoptotic pathway. Lab Invest. 2017;97:792-805 pubmed publisher
    ..Exposure of cultured rat β-cells (INS-1) to AOPPs induced an increase in Bax expression, caspase-3 activity, and apoptosis as well as a decrease in Bcl-2 expression in a dose- and time-..
  52. Samoilov M, Sitnik N, Rybnikova E, Gluschenko T, Tjulkova E. The expression pattern of pro- and antiapoptotic proteins bax and Bcl-2 in rat brain neurons in response to severe hypobaric hypoxia: the correcting effect of hypoxic preconditioning. Dokl Biol Sci. 2005;402:176-8 pubmed
  53. Zeng Q, Oakley B. p53 and Bax: putative death factors in taste cell turnover. J Comp Neurol. 1999;413:168-80 pubmed
    ..to seek putative death factors, we observed that squamous epithelial cells of the tongue were negative for Bax, a death factor in the Bcl-2 family of survival/death factors, and were also negative for p53, a tumor-suppressor ..