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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
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Bid (show BID Proteins) 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 (show BCL2 Proteins) expression and gene transcription, enhancing production of virus progeny, but does not increase Bax expression.
It was concluded that the Fas (show FAS Proteins)-FasL (show FASL Proteins) signaling pathway was involved in regulation of bovine oocyte apoptosis, perhaps related to B (show TDO2 Proteins) cell lymphoma/leukemia-2 associated X upregulation.
apoptosis-inducing factor (show AIFM1 Proteins) was expressed in luminal alveolar cells and, in concert with a change in bax protein to bcl-2 (show BCL2 Proteins) 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 (show BCL2 Proteins), caspase-3 (show CASP3 Proteins) and-7 cannot be used as a reliable apoptosis detection method.
The effect of culture conditions on expression of heat shock protein 70 (show HSP70 Proteins) 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 (show TP53 Proteins) activity in promoting hair cell death due to aminoglycosides, likely upstream of Bax and Bcl2 (show BCL2 Proteins).
The proapoptotic BCL-2 (show BCL2 Proteins) proteins BAX and BAK (show BAK1 Proteins) can commit a cell to its programmed death by permeabilizing the outer mitochondrial membrane and subsequent initiation of the caspase (show CASP3 Proteins) cascade. (Review)
Bax activator BTC (show BTC Proteins)-8 inhibited glioblastoma (GBM) cell proliferation, arrested the cell cycle, and induced apoptosis through the induction of mitochondrial membrane permeabilization. Most importantly, BTC (show BTC Proteins)-8 blocked proliferation and self-renewal of glioma stem cells (GSC (show GSC Proteins)) and induced their apoptosis. BTC (show BTC Proteins)-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 (show CGA Proteins))suppresses hLECs apoptosis and prevents lens opacity induced by H2O2 via Bax/Bcl2 (show BCL2 Proteins) signaling pathway. CGA (show CGA Proteins) 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 (show BCL2 Proteins) and p53 (show TP53 Proteins)/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 (show VDAC2 Proteins) ensures mitochondria-specific membrane association of Bax and in the absence of VDAC2 (show VDAC2 Proteins) 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 (show VDAC2 Proteins) 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 (show HGF Proteins) 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 (show CYCS Proteins) in atomic detail
Study reports the proximal alpha1-alpha2 loop as a second activation site in Bak (show BAK1 Proteins) and in mitochondrial Bax.
T-2 toxin appears to activate specific intracellular death-related pathways leading to Bax-dependent caspase-3 (show CASP3 Proteins) 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 (show BCL2 Proteins), and maintains the osteoblastic function of MC3T3E1 cells following GC exposure. In addition, these results indicated that the suppression of autophagy in OBs (show LEP Proteins) 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 (show BAK1 Proteins) 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 (show CARS Proteins) die in a Bax-dependent manner. Bax-inactivated rescued septum-CRs (show CARS Proteins) 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 (show BAK1 Proteins)-caspase (show CASP3 Proteins) signaling cascade. Adult Bax/Bak (show BAK1 Proteins) 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.
These results suggest that Bax mediates beta-cell apoptosis in Pdx1 (show PDX1 Proteins)-deficient diabetes.
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 (show BCL2 Proteins).
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 (show BCL2 Proteins) 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 (show BCL2 Proteins) and bax were expressed strongly in denervated guinea-pig facial muscle. [bcl-2 (show BCL2 Proteins); bax]
goat oocytes based on G6PDH (show G6PD Proteins)-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 (show BCL2 Proteins) ).
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