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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 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.
Similarities were found in the crystal structures of wild-type and BAX P168G mutation but significant other differences suggest that cytosolic BAX exists as an ensemble of conformers which distribution within the ensemble determines the different functions of wild-type and mutant proteins. Other data with BAX inhibition argue for an allosteric model of BAX regulation that derives from properties of the ensemble.
cardiolipin has an important role in determining the formation of active BAX oligomers
These data reveal that miR-29a/Bax axis plays an important role in regulating chondrocyte apoptosis and suggest that targeting the proapoptotic protein Bax and increasing expression levels of miR-29a emerge as potential approach for protection against the development of Osteoarthritis.
miR-339-5p promotes proliferation and survival of Stem Cell Leukemia/Lymphoma Syndrome cells through downregulation of the BCL2L11 and BAX pro-apoptotic genes
Levels of IL-1ss, IL-6, TNF-alpha, and BAX mRNA were negatively correlated with cardiac function, and BCL2 mRNA expression was positively associated with chronic heart failure.
The reduction in mitochondrial membrane potential favored mitochondrial apoptotic pathway which was further confirmed by determining the expression of Bax and Bcl-2. It was observed that MH downregulated the expression of Bax and upregulated the expression of MMP, ultimately leading to apoptosis of OSSC PE/CA-PJ41 cells. Additionally, MH also caused G2/M cell cycle arrest in a dose-dependent manner.
Silencing of miR-19a significantly improved the sensitivity of SiHa cells to radiotherapy by reducing proliferation, increasing apoptosis, upregulating BAX, and downregulating Bcl-2. Overall, inhibiting miR-19a significantly improves the sensitivity of SiHa cells to radiotherapy, which could lead to new methods for the treatment of cervical cancer.
The results of the present work revealed that aesculetin exhibits selective anticancer effects in THP-1 human leukemia cells without causing much cytotoxicity in peripheral blood mono-nucleated cells. It also led to significant apoptosis induction, inhibition of cancer cell migration and decrease in Blc-2/Bax ratio.
Results found that Bax mRNA expression in the exposed group were significantly higher than that in the control group. The levels of gene expression were positively correlated with the concentrations of urinaryinorganic arsenic, monomethylarsonic acid and dimethylarsinic acid in all subjects.
Ag/Au bimetallic nanoparticles induce apoptosis in human cancer cell lines via P53, CASPASE-3 and BAX/BCL-2 pathways.
Results demonstrated that the pro-apoptotic Bax promotes promotes mesenchymal-epithelial transition by binding to complex-I, antagonizing the epithelial-mesenchymal transition inducing functions of pro-survival Bcl-2 proteins.
Venetoclax/GDC-0980 activity was partially diminished in BAK(-/-) cells.
Phosphorylation by Akt converts the pro-apoptotic protein Bax into an anti-apoptotic protein. Phosphorylated anti-apoptotic Bax promotes resistance of cancer cells to inherent and drug-induced apoptosis.
In a compairison of endometrial neoplasms to non-malignant conditions (including endometrial hyperplasia), in endometrial neoplasms, p53 is over-expressed, Bax is under-expressed and the Bcl2 to Bax ratio is higher.
Transfection with the BANCR expression vector significantly inhibited proliferation and promoted apoptosis of KGN cells, and significantly promoted the expression levels of proapoptotic Bax and p53. Therefore, it may be concluded that lncRNA BANCR participates in PCOS by promoting cell apoptosis through the upregulation of Bax and p53.
These results suggest that overexpression of miR-573 inhibited nucleus pulposus cell apoptosis by down-regulating Bax.
The study shows complex interrelation between apoptosis and cell cycle regulating proteins (MDM2, BCL2 and Bax) in benign prostatic hyperplasia and prostate cancer.
Expression of MDM2 and Bcl2 was significantly up-regulated, while Bax was down-regulated in renal cell carcinoma as compared with normal kidney tissue.
Positive and negative correlations were found between serum Bcl-2, Bax, Bcl-2/Bax ratio and HCV viral load in non-cirrhotic and cirrhotic patients respectively. These findings provide an evidence that apoptosis is dysregulated in patients with chronic Hepatitis C.
Lower expression of Bax predicts poor clinical outcome in patients with glioma after curative resection and radiotherapy/chemotherapy.
Data demonstrate a role for SNAP23 in the control of adipocytemacroautophagy and programmed cell death through an ATG9-dependent, but ATG7-independent, pathway regulating BAX protein levels and BAX activation.
The results suggest that BAX can regulate the survival of Nestin-expressing cells but other factors control the fate choice.
6 months of aerobic exercise can effectively prevent cardiomyocyte apoptosis in mice. It is an important way to effectively regulate Bcl-2, Bax expression and Bcl-2/Bax level of cardiomyocytes.
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.
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