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Human BAX Protein expressed in Wheat germ - ABIN1346446
Kim, Kim, Park, Hwang, Kim, Lee, Kang, Um: Bcl-w promotes cell invasion by blocking the invasion-suppressing action of Bax. in Cellular signalling 2012
Show all 3 Pubmed References
Bid and Bax are signal transduction factors in granulosa cells and play proapoptotic roles.
The data demonstrate that severe hypocapnia results in increased Bax expression, DNA fragmentation, and membrane lipid peroxidation in mitochondria of cerebral cortical neurons of newborn piglets, and may result in apoptotic cell death.
BoHV-5 replication apparently modulates BCL-2 expression and gene transcription, enhancing production of virus progeny, but does not increase Bax expression.
It was concluded that the Fas-FasL signaling pathway was involved in regulation of bovine oocyte apoptosis, perhaps related to B cell lymphoma/leukemia-2 associated X upregulation.
apoptosis-inducing factor was expressed in luminal alveolar cells and, in concert with a change in bax protein to bcl-2 protein ratio, might contribute to signalling of a change in the dynamic balance of the cell population as lactation progresses
mRNA expression of Bax, Bcl-2, caspase-3 and-7 cannot be used as a reliable apoptosis detection method.
The effect of culture conditions on expression of heat shock protein 70 and Bax protein in bovine blastocysts is reported.
xlbax is a regulator of muscle fiber death in the regressing tail during metamorphosis.
These results suggest a role for mitochondrial p53 activity in promoting hair cell death due to aminoglycosides, likely upstream of Bax and Bcl2.
energy landscape of BIM (BH3-only peptide) induced BAX activation has been computed, and the molecular origin of those events is hereby reported in atomistic detail
Immunohistochemical staining results showed that the expression of Bax, Bax/Bcl-2, TGF-beta1, and type III collagen in the experimental group was significantly increased compared to the control group (p<0.01).
Pro-apoptotic protein Bax is main effector of mitochondrial permeabilization during apoptosis. Data suggest Bax N-terminal acetylation by mouse NatB (or yeast Naa20p) is involved in mitochondrial targeting of Bax. These studies used recombinant human Bax expressed in yeast cells plus cultured embryonic cells from knockout, transgenic, and chimeric mice. (NatB and Naa20p = N-terminal acetyltransferases)
This result suggests that p53 has an important role in hemangioma endothelial cell (HemEC) apoptosis. The results of the present study additionally suggest that the propranololinduced HemEC apoptosis pathway is a mitochondrial apoptosis pathway and is regulated by p53BAX signaling.
The results of the present study revealed that the combination of P. gingivalis and H1N1 infection in lung epithelial cells may promote the production of inflammatory cytokines and increase NO production, leading to increased levels of apoptosis in lung epithelial cells via the Bcl2/Bax/caspase3 signaling pathway.
The proapoptotic BCL-2 proteins BAX and BAK can commit a cell to its programmed death by permeabilizing the outer mitochondrial membrane and subsequent initiation of the caspase cascade. (Review)
Bax activator BTC-8 inhibited glioblastoma (GBM) cell proliferation, arrested the cell cycle, and induced apoptosis through the induction of mitochondrial membrane permeabilization. Most importantly, BTC-8 blocked proliferation and self-renewal of glioma stem cells (GSC) and induced their apoptosis. BTC-8 was demonstrated to sensitize both GBM cells and GSCs to the alkylating agent Temozolomide.
BAX nuclear localization was associated in vivo with the remodelling of lung parenchyma during development, tumorigenesis as well as fibrosis compared to control adult human lungs
There is no significant association between BAX gene polymorphism and cancer susceptibility, but it probably contributes to increased adverse prognosis to cancer.
These results suggest that chlorogenic acid (CGA)suppresses hLECs apoptosis and prevents lens opacity induced by H2O2 via Bax/Bcl2 signaling pathway. CGA may provide effective defenses against oxidative stress and, thus, has potential as treatment for a variety of diseases in clinical practice.
Ru(II)/diphenylphosphine/pyridine-6-thiolate complexes induce S-180 cell apoptosis through intrinsic mitochondrial pathway involving inhibition of Bcl-2 and p53/Bax activation.
helix alpha9 assists Bax activation via the dimer heterogeneity and interactions with specific MOM lipids, which eventually facilitate proteolipidic pore formation in apoptosis regulation
VDAC2 ensures mitochondria-specific membrane association of Bax and in the absence of VDAC2 Bax localizes towards other cell compartments. Bax retrotranslocation is also regulated by nucleotides and calcium ions, suggesting a potential role of the transport of these ions through VDAC2 in Bax retrotranslocation.
The results of the genes expression analysis revealed that indocyanine green-photodynamic therapy at concentrations 1000mug/mL, induced the significant expression of BAX in HGF cells
Our observations point to misfolded Bax states, shedding light on the molecular mechanism of Bax mutation-elicited cancer. Most importantly, the structure of the Bax pore facilitates future study of releases cytochrome C in atomic detail
Data suggest that regulation of pancreatic beta-cell function and survival/apoptosis involves alternative splicing modulated by key splicing regulator SRP55; SRP55-regulated alternative splicing includes modulation of function of pro-apoptotic proteins (BIM, BAX), JNK signaling, and endoplasmic reticulum stress. (SRP55 = pre-mRNA-splicing factor SRP55; BIM = BCL-2 interacting protein BIM)
High expression of BAX is associated with colorectal cancer.
High mitochondrial Bax apoptosis regulator protein (BAX) levels correlate with improved acute myeloid leukemia (AML) patient survival.
parkin-dependent targeting of misregulated BAX on the mitochondria provides substantial protection against BAX apoptotic activity.
our data present preliminary evidence that inherited abnormalities in the intrinsic apoptosis pathway, related to BAX G(-248)A and BCL2 C(-717)A SNPs, are associated with treatment response and act as independent prognostic factors in DLBCL.
These results show that the levels of AMTN mRNA induced by TGFbeta1 and Smad3 are decreased by robust expression of Bax in gingival epithelial cells.
Our results show that reprogramming is enhanced in MEFs deficient in BAK and BAX, but only when MYC is part of the reprogramming cocktail. Thus, the propensity for Myc overexpression to elicit apoptosis creates a significant roadblock to reprogramming under OKSM conditions.
VDAC2 phenocopied the loss of BAX in impairing both the killing of tumor cells by anti-cancer agents and the ability to suppress tumor formation.
It was shown that double knockout of Bax and Bak from proximal tubules attenuated renal tubular cell apoptosis and suppressed renal interstitial fibrosis in UUO.
Study reports the proximal alpha1-alpha2 loop as a second activation site in Bak and in mitochondrial Bax.
T-2 toxin appears to activate specific intracellular death-related pathways leading to Bax-dependent caspase-3 activation and the induction of apoptosis in Leydig cells.
The data revealed that autophagy is an important regulator of osteoblastic apoptosis through its interaction with Bax/Bcl2, and maintains the osteoblastic function of MC3T3E1 cells following GC exposure. In addition, these results indicated that the suppression of autophagy in OBs under chronic GC therapy may increase the prevalence of GCinduced osteoporosis and fragility fractures.
Here the authors show that mouse embryonic fibroblasts deficient in Bax/Bak1 are resistant to the third major form of cell death associated with autophagy through a mechanism involving lysosome permeability.
although all CR subtypes undergo cell death, septum, but not hem, CRs die in a Bax-dependent manner. Bax-inactivated rescued septum-CRs maintain immature electrophysiological properties
An autoinhibited dimeric form of BAX regulates the cytosolic BAX activation pathway.
Postnatal synaptic rearrangement needed for acquisition of skilled behaviors requires the activity-dependent, non-apoptotic Bax/Bak-caspase signaling cascade. Adult Bax/Bak mutant mice exhibit aberrant co-activation of antagonistic muscle pairs and skilled grasping deficits but normal reaching and retrieval behaviors.
Study found that emphysema occurred in ku70(-/-) mice at the age of three-months old, and that Bax deficiency was able to suppress it. These results suggest that Bax-mediated apoptosis induces emphysema in ku70(-/-) mice.
The polyglutamine embedded in the ER membrane was observed at the same time as Bax insertion. These results demonstrated that the ER membrane may be a target of polyglutamine, which triggers cell death through Bax.
Its gene expression is up-regulated by hyperoxia.
These results suggest that Bax mediates beta-cell apoptosis in Pdx1-deficient diabetes.
Bim and Puma overlapped apoptosis only partially during physiological apoptotic stage and they were present in non-apoptotic parts of the follicles.
This study demonstated that Bax KO mice show Hyperactivity and depression.
The influence of chronic ethanol consumption on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes was studied in the brain structures of B6-1473C (C/C) and B6-1473G (G/G) mice that had been obtained on the base of the C57BL/6 strain.
These data indicate that the rapid and robust microglial activation and PIF expression observed in situ following acute EtOH exposure is largely driven indirectly by BAX-dependent apoptotic cell death, rather than directly by the EtOH.
lipid profile in the absence of the proapoptotic proteins BAX and BAK in mouse embryonic fibroblasts
The content of Bax protein in the cardiomyocyte cytoplasm decreased, thus indicating that the mitochondrial pathway was not involved in the realization of the apoptotic program in a model of ventricular overload.
These results indicate that RI-PostC can ameliorate myocardial ischemia-reperfusion injury and increase the Bcl-2/Bax ratio through a mechanism involving protein kinase C.
Cinobufagin can remarkably inhibit the proliferation and induce the apoptosis of lens epithelial cells by increasing expression of bax and decreasing expression of bcl2.
Elevated local temperature of the testis buried in the inguinal pocket increases the apoptosis of spermatogenic cells, and the spermatogenic cell apoptosis is highly correlated with the decreased expression of Bcl-2 and increased expression of Bax.
In this study evidence is provided that exogenous PGF2alpha differentially modulates luteal expression of BCL2-associated X protein (BAX) transcripts and protein depending on luteal stage.
bcl-2 and bax were expressed strongly in denervated guinea-pig facial muscle. [bcl-2; bax]
goat oocytes based on G6PDH-activity through the BCB test improves their developmental competence, increases intracellular GSH content, and affects the expression of the apoptosis-related genes9 Bax and Bcl-2 ).
The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to the loss in membrane potential and the release of cytochrome c. The expression of this gene is regulated by the tumor suppressor P53 and has been shown to be involved in P53-mediated apoptosis. Multiple alternatively spliced transcript variants, which encode different isoforms, have been reported for this gene.
BCL2-associated X protein
, BCL2-associated protein
, apoptosis regulator BAX
, bax zeta
, BCL2-associated X protein omega
, BCL2-associated X protein transcript variant delta2
, bcl-2-like protein 4