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Validated All-in-One™ qPCR Primer for BAX(NM_004324.3) Search again
Product ID:
HQP015964
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BCL2L4
Gene Description:
BCL2 associated X, apoptosis regulator
Target Gene Accession:
NM_004324.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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.
Gene References into function
- Gamma-radiation-induced apoptosis of leukemia cells was associated with activation of multiple caspases and bax up-regulation as determined by RNase protection assays. TLCK prevented bax up-regulation as a result of its inhibitory effect on p53 function.
- expression is related to apoptosis in thymus
- an elevated bcl-2/bax ratio in rectal carcinoma tissue specimens suggests increased tumor resistance to adjuvant radiotherapy
- Bax-dependent release of Smac/DIABLO from mitochondria mediates death receptor-mediated apoptosis
- Sanguinarine-treated K562 human cells showed a significant increase in expression of the pro-apoptotic Bax protein in apoptosis.
- BAX expression in Hodgkin and Reed-Sternberg cells of Hodgkin's disease: correlation with clinical outcome
- Protein kinase A RIalpha antisense inhibition of PC3M prostate cancer cell growth: Bcl-2 hyperphosphorylation, Bax up-regulation, and Bad-hypophosphorylation
- The phosphatidylinositol 3-kinase (PI3K)-Akt pathway suppresses Bax translocation to mitochondria
- conserved intronic response element mediates direct p53-dependent transcriptional activation of bax gene
- Curcumin induces apoptosis in human breast cancer cells through p53-dependent Bax induction.
- analyzed expression in leiomyomas and myometrium from fertile and menopausal women
- the expression of apoptosis-regulating proteins BAX in patients with Burkitt's lymphoma, expression of pro-apoptotic proteins could provide BL cells ability to undergo apoptosis after chemotherapy.
- Results show that Bax is essential for death receptor-mediated apoptosis in cancer cells; it is also involved in mitochondrial changes and downstream caspase activation.
- Bax induction triggers apoptosis by initiating caspase activation not mediated by mitochondrial cytochrome c release and mitochondrial membrane potential change in K562 cells
- Bcl-2 expression was not related with any pathological parameters: size, nuclear grade and stage or prognosis in renal cell carcinmoma
- mediation of Ca2+ mobilization promotes cytochrome c release during apoptosis
- Expression of apoptotic regulators and their significance in cervical cancer
- BAX is required for TRAIL/Apo2L-induced apoptosis of colorectal cancers: synergism with sulindac-mediated inhibition of Bcl-x(L).
- data suggest that oxidation of extracellular matrix proteins may enhance human mesangial cell apoptosis via a mechanism that appears to involve enhanced expression of Bax and caspase activation
- Bcl-2 family member Bfl-1/A1 sequesters truncated bid to inhibit is collaboration with pro-apoptotic Bak or Bax.
- limits Adenovirus replication through apoptosis induction
- Peg3/Pw1 is a mediator between p53 and Bax in DNA damage-induced neuronal death
- expression of apoptosis-regulating proteins p53, Bcl-2, and Bax in primary resected esophageal squamous cell carcinoma
- disrupted p53/BAX pathway is associated with a poor clinical outcome in UICC III tumors
- Identification of novel isoforms of the BH3 domain protein Bim which directly activate Bax to trigger apoptosis.
- activation during apoptosis due to oxidative stress in cells expressing wild-type and mutant cystic fibrosis transmembrane conductance regulator
- high Bax expression associated with apoptosis in renal cell carcinoma
- Involvement of nuclear factor-kappa B, Bax and Bcl-2 in induction of cell cycle arrest and apoptosis by apigenin in human prostate carcinoma cells
- Defective Bax activation in Hodgkin B-cell lines confers resistance to staurosporine-induced apoptosis
- Studies of the mechanism of CD40-mediated apoptosis of human Burkitt lymphoma cell lines revealed an increase in bax messenger RNA with a subsequent increase in Bax protein in the mitochondria.
- BAX translocation and conformation changes are necessary for TRAIL-induced apoptosis.
- Inactivation of p21WAF1 sensitizes cells to apoptosis via an increase of both p14ARF and p53 levels and an alteration of this protein and Bcl-2 ratio
- Bcl-2 proto-oncogene proteins are expressed in Meissner corpuscles and may play a role in resistance to apoptosis.
- A mitochondrial matrix targeting signal can override the inhibition of import of Bax in the absence of apoptotic stimulus. Truncated variants of Bax cause apoptosis when targeted to mitochondria by cytochrome c release from an ectopic environment.
- conformational changes of Bax are among the early steps in the induction of cell death
- Retinoids cause apoptosis in pancreatic cancer cells via activation of RAR-gamma and altered expression of Bcl-2/Bax.
- Bax oligomerization in mitochondrial membranes requires tBid (caspase-8-cleaved Bid) and a mitochondrial protein
- During endothelial cell apoptosis, Bax protein was upregulated in HUVECs stimulated with TNF-alpha alone or in combination with IFN-gamma.
- the role of nitric oxide and death regulatory genes, bcl-2 and bax, in human endometria apoptosis
- Differential rates of frameshift alterations in four repeat sequences of hereditary nonpolyposis colorectal cancer tumors.These repeats consisted of (A)10 in the TGF beta RII, (G)8 in the BAX, (A)8 in the CASP1, and (CCA)7 in the APP genes.
- Immunohistochemical expression of this protein in squamous cell carcinomas from immunosuppressed renal transplant recipients and immunocompetent individuals.
- Polymorphism in bax protein is associated with chronic lymphocytic leukemia
- part of the mechanism utilized by the adenovirus E1B-19K protein to suppress apoptosis during adenovirus infection may involve modulation of the activities of BAX
- Independent predictor of a favourable prognosis in urinary bladder cancer
- Regulation of intracellular pH mediates Bax activation in HeLa cells treated with staurosporine or tumor necrosis factor-alpha
- Apocytochrome c blocks caspase-9 activation and Bax induced apoptosis
- Overexpression of Bax is able to sensitize HCC-9204 cell apoptosis induced by a driamycin
- Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane
- interaction with and regulation by 14-3-3
- A very low mRNA level was indicated at bax, bcl-2 and bcl-xL in hepatocellular carcinoma tissues in contrast to normal liver.
- In Bax+/+, axotomy of the sciatic nerve induced significant cell loss in the pool. Most motoneurons survived axotomy in Bax-/-, although they appeared atrophic and their AChE expression was decreased.
- functional cooperation between Bax and Bak in cell hypoxia, an absolute requirement of Bax for mitochondrial permeabilization
- Bcl-2 on the endoplasmic reticulum regulates this protein's activity by binding to BH3-only proteins.
- BAX epression in B-CLL cells is a critical factor in promoting apoptosis, but probably not by repression of BCL2 gene transcription.
- Calpain-induced Bax-cleavage product is a more potent inducer of apoptotic cell death than wild-type Bax. The cleavage site was between Gln28 and Gly29
- In PC-3/bcl-2 transfectants, DX exposure after IR caused an induction of BAX/
- Drp1 and Mfn2, but not other proteins implicated in the regulation of mitochondrial morphology, colocalize with Bax in apoptotic foci
- the p38MAPK activation-Bax expression pathway might be involved in apoptosis induced by oxidative stress
- Intact BAX expression levels decreased when H202 was greater than 250 micro M. The cleaved form of BAX appeared prior to caspase-3 activation, increasing in a dose-dependent manner.
- Bax, Bcl-2, fas and Fas-L antigen expression in human seminoma: correlation with the apoptotic index.
- Proapoptotic genes BAX and CD40L are predictors of survival in transitional cell carcinoma of the bladder.
- Poly(ADP-ribose) polymerase activation and changes in Bax protein expression associated with extracellular ATP-mediated apoptosis in human embryonic kidney 293-P2X7 cells.
- Bax interacts with humanin (HN), an anti-apoptotic peptide of 24 amino acids encoded in mammalian genomes
- Deletions of 1p were found in 12/56 adenomas and, seemingly, most frequent in patients with few tumours. The most frequently expressed protein was BAX (33/41), but neither this nor the other proteins showed associations with an in situ growth pattern.
- p53 accumulation and loss of bax expression influence the acquisition of a malignant phenotype but seem to have no further impact on tumor progression.
- bax should be considered as independent biologic prognostic parameter in diffuse large B-cell lymphoma, thereby aiding in the identification of patient risk groups.
- Cat D triggers Bax activation, Bax induces the selective release of mitochondrial AIF, and the latter is responsible for the early apoptotic phenotype in T-cells
- Bax and Bak have roles in Bid-mediated apoptosis
- although cleavage to p18 Bax is not required for Bax to initiate apoptosis, p18 Bax potently accelerates the apoptotic process.
- BAX protein expression was elevated upon RFN36 induction in test cells.
- NBK mediated apoptosis entirely by BAX-dependent mitochondrial pathway.
- Bax siRNA significantly prevents apoptosis. Together with a dominant-negative death receptor DR5, it completely blocked apoptosis, indicating the essential role of mitochondrial and receptor-mediated apoptotic pathways activated by Apo2L/TRAIL and CPT-11
- BAX has a role in cell death in human primary neurons, but its action is inhibited by cytosolic prion protein
- p21WAF1/CIP1, pRB, Bax and NF-kappaB have roles in induction of growth arrest and apoptosis by resveratrol in tumor cell lines
- our data suggest that an association of PKCepsilon with Bax may neutralize apoptotic signals propagated through a mitochondrial death-signaling pathway.
- demonstrate that Bax is sensitized to activation by transient interaction with lipid membrane surfaces and provide evidence that Bax activation proceeds in a stepwise fashion, with multiple triggers and potential levels of regulation
- PUMA-induced Bax conformational change and Bax translocation to mitochondria can be separate events and the conformational change in Bax is crucial for PUMA-induced mitochondrial dysfunction
- Bax may not play a direct role in the genesis of ovarian endometrioid carcinoma, regardless of microsatellite instability status.
- BAX expression by midbrain neurons was confirmed by immunoblot analysis on SN extracts showing a specific band of approximately 21kDa, which is consistent with the known molecular weight of native BAX.
- Bcl-2/Bax may be involved, at least in part, in the apoptotic activity in extrahepatic biliary carcinoma.
- the cascade of pro-apoptotic events leading to Bax, mitochondria, and caspase-3 activation are regulated by calpastatin and calpain-1
- bax has a role in beta-sitosterol-mediated apoptosis in human colon cancer cells
- Abnormal Bcl-2 and Bax protein bands after induction therapy in AML patients may be considered as factors associated with unfavorable clinical outcome.
- Bcl-x:Bax ratio was associated with survival in thymic neuroendocrine tumors.
- findings demonstrate that p73 protein elicits apoptosis via the mitochondrial pathway using p53 up regulated modulator of apoptosis(PUMA) and Bax protein as mediators
- Human prolactin-G129R-induced breast cancer cell and/or mammary gland apoptosis which is mediated, at least in part, through the regulation of Bax and Bcl-2 gene expression.
- Bax plays an important role in UV-induced apoptosis and in caspase-2 activation.
- An activated form of Bax alpha causes an increase in the rate of lipid transbilayer diffusion such as occurs upon initiation of apoptosis, when there is a net movement of cardiolipin to the surface of mitochondria.
- role of p18(Bax) in apoptosis and found that its activity required the presence of p21(Bax)
- The expression of estrogen receptor alpha, progesterone receptor, bax protein, and Bcl-2 protein changed parallel with that of Akt protein.
- Both benign and malignant diseased gallbladder wall expressed iNOS and Bax
- H pylori may enhance Bid, Bax and Bcl-2 mRNA levels and cause deregulation of these apoptosis-associated genes expressions, which may play a role during development of gastric adenocarcinoma induced by H pylori.
- Assessment of p21, p27, Bax, and cyclin E expression in tumor tissues have been reported to be useful as prognostic factors in head and neck squamous cell carcinoma.
- Results suggest that apoptosis-associated speck-like protein (ASC) can function as an adaptor molecule for Bax and regulate a p53-Bax mitochondrial pathway of apoptosis.
- Bax is regulated by phosphorylation of Ser(184) in an Akt-dependent manner and that phosphorylation inhibits Bax effects on the mitochondria by maintaining the protein in the cytoplasm, heterodimerized with antiapoptotic Bcl-2 family members.
- Bax and Bcl-2 proteins are elevated after treatment with cladribine, cyclophosphamide, mitoxantrone, and combination chemotherapy
- p53 directly activated the proapoptotic Bcl-2 protein Bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program
- Bcl-2 and bax molecules play a role in the regulation of apoptotic mechanisms in pituitary adenomas.
- Data show that oxygen deprivation cancer cells provoked decreased mRNA and protein levels of proapoptotic Bid and Bad, and that hypoxia-inducible factor 1 (HIF-1) was dispensable for the down-regulation of Bad but required for that of Bid.
- Pro168 links the NH2 and the COOH terminus of Bax and is required for COOH-terminal release and mitochondrial targeting once this link is broken.
- Bax transcription is regulated by HNRNP associated with YAP
- Cytomegalovirus cell death suppressor vMIA binds Bax
- survivin, p53, and bcl-2 are elevated in breast carcinoma but not ductal intraepithelial neoplasia
- reduced expression of Bax might play a role in resistance to various apoptosis-inducing stimuli in HL-CR cells
- BCR-signal causes Bax translocation, followed by mitochondrial depolarization, and cytC release
- Daxx501-625-induced apoptosis is mediated through the ASK1-MEK-JNK/p38-Bim-Bax-dependent caspase pathway
- p53 acts upstream of Bax to promote antineoplastics mediated cell death in a proline-rich domain-dependent manner through both transcription-dependent and -independent mechanisms in human colon cancer HCT116 cells.
- A significant increase in p16(INK4A) and Bax expression was found in ulccerative colitis-associated tumors.
- Alteriations of BAX are not responsible for cancers in TP53 wild-type Li-Fraumeni syndrome families.
- Bcl-2 interacts with activated Bax during apoptosis in an effective manner to neutralize the proapoptotic activity of Bax.
- the activated PKCdelta catalytic domain triggered the redistribution and activation of Bax
- Down Regulation of Bax protein is associated with benign prostatic hyperplasia
- Activation of Bax was inhibited in Chlamydia trachomatis infected Hela cells.
- evaluated the expression of Bcl-2, Bax and Bak in patients with Graves Disease (GD); findings suggest that the differential expression of Bcl-2 family proteins in both thyrocytes and lymphoid follicles may be involved in the pathology of GD
- results demonstrate that translocation of Bax from the cytosol to the mitochondrial membrane occurred under hypoxia, thereby leading to pathological tissue destruction
- role of Bax in radiation sensitivity in esophageal carcinoma cells
- the conformation of the BAX alpha9-helix plays a significant role in BAX/BCL-xL interaction
- establish distinct roles for Bax and Bak in linking the TRAIL death receptor pathway to the mitochondrial apoptosis signaling cascade and delineate a higher degree of specificity in signaling for cell death by multidomain Bcl-2 homologs
- aberrant ratio of bcl-2 to bax protein expression may be involved in the course of tumorigenesis of cholangiocellular carcinoma
- results suggest that the generation of ceramide in mitochondria in response to TNFalpha is sufficient to induce Bax translocation to mitochondria and subsequent cytochrome c release and cell death
- a specific interaction between Bax Halpha1 and their BH3 domains allows Bid and PUMA to function as "death agonists" of Bax
- inhibition of Bax may be an important antiapoptotic activity of LMP-1 of Epstein-Barr virus
- The optic nerve axons in glaucomatous eyeballs showed statistically significant higher Bax protein expressions than those of Bcl-2 proteins.
- nicotine-induced survival and chemoresistance of human lung cancer cells may occur in a novel mechanism involving activation of PI3K/AKT that directly phosphorylates and inactivates the proapoptotic function of Bax
- The regulation and control of gastrin, somatostatin in cell apoptosis of large intestine carcinoma may be directly related to the abnormal expression of bcl-2, bax.
- The increased ratio of Bax/Bcl-2 proteins after Epigallocatechin-3-gallate may have resulted in increased release of cytochrome c from mitochondria into cytosol.
- G125A polymorphism reduced expression of the BAX promoter by 2.6-fold.
- The preliminary results of cDNA microarray analysis showed the down-regulation of anti-apoptotic Bcl-xL and up-regulation of pro-apoptotic Bax in the process of 15d-PGJ(2)-induced apoptosis.
- Arsenic trioxide might exert cell killing in part by inducing Bax activation through a Bcl-2-suppressible pathway in hematopoietic cells that is caspase independent and intracellular ROS regulated
- P21 and Bax have roles in progression of cutaneous malignant melanoma
- results suggest that UV light-triggered acid sphingomyelinase activation is essentially required for Bax protein conformational change leading to mitochondrial release of pro-apoptotic factors
- VDAC-2 inhibits the Bak-mediated apoptotic response via Bax
- demonstrated that epigallocatechin-3-gallate activates growth arrest and apoptosis primarily via tumor suppressor p53-dependent pathway that involves the function of both p21 protein and Bax protein
- AR and IGF1 cooperate to prevent apoptosis by activating a specific PKC-p90(rsk)-dependent pathway, which leads to Bad and Bax inactivation.
- Expression of Cx26, Bax and Bcl-xL in colorectal cancers. Association of Cx26, Bax and Bcl-xLwith histological G2 grade of tumors.
- In the exone 3 of the gene Bax mutation G7/G9 in cells SKOV3 results in an inactivation of proapoptotic activity of the protein Bax.
- Rapamycin induces apoptosis of tumor cells by increasing the ratio of Bax to Bcl-xL through mechanisms dependent and independent of its mTOR inhibitory activity
- roles for Bax and Bak in linking the TRAIL death receptor pathway to the mitochondrial apoptosis signaling cascade upon DNA damage by ionizing radiation.
- Bax expression is comparable in verrucous and low-grade squamous cell penile carcinomas.
- p53, Bax, Bcl-2 and Mdm2 mRNA expression levels correlate with the malignant transformation of the uterine cervix
- in HeLa cells, both Smac and Cyt-c are released from mitochondria during UV-induced apoptosis through the same permeability transition mechanism triggered by aggregation of Bax
- Prion protein (PrP) prevents Bcl-2-associated protein X (Bax)-mediated cell death.PrP protects against Bax-mediated cell death by preventing the Bax proapoptotic conformational change that occurs initially in Bax activation
- Bax but not Bcl-2 expression is increased after exposure to prostaglandin A2 and 2-methoxyestradiol in Hela cells
- The tumor suppressor gene RASSF1A is required for death receptor-induced Bax conformational change and apoptosis.
- Overexpression of Bax not only induces apoptosis, but also sensitizes hepatoma cells to cell death induced by adriamycin.
- Bax gene therapy with cationic liposomes will be useful for osteosarcoma.
- Bcl-xL/Bax ratio can block the apoptotic response in TNFalpha-stimulated cells but allows cell death initiation when it is altered by a crosstalk between IFNgamma presensitization and TNFalpha induced signaling.
- Taken together, our results suggest that the elevated level of clusterin in human cancers may promote oncogenic transformation and tumour progression by interfering with Bax pro-apoptotic activities.
- overexpressing an antioxidant gene such as GPX1 in endothelial cells is able to change the basal mRNA and protein Bax levels without affecting those of p53 and Bcl-2
- Spontaneous apoptosis is reduced in the endometrium of unexplained-infertile women, and is associated with the changed Bcl-2:Bax ratio.
- Bax, Bad, and Bim are upregulated, while Bcl-2 is downregulated in human neuroblastoma cells treated with propargylamine
- Hsp70 blocks heat-induced apoptosis primarily by inhibiting Bax activation and thereby preventing the release of proapoptotic factors from mitochondria
- proteolytic activation of Bid and the subsequent induction of the mitochondrial apoptotic pathway through Bax/Bak is essential for apoptosis triggered by caspase-2
- Data evaluate and compare the bcl2, bax, and nestin patterns in the frontal cortices of Alzheimer and multiple-infarct dementia patients, and in normal aging.
- To evaluate the importance of Bax in apoptosis after photodynamic therapy (PDT), we compared the PDT responses of Bax-proficient (Bax(+/-)) and Bax knock-out (BaxKO) HCT116 human colon cancer cells.
- Blockade of Bax by using anti-Bax small interfering double stranded RNA (siRNA) significantly reduced gefitinib-induced apoptosis. Taken together, these data suggest a critical role of p18 Bax in gefitinib-induced apoptosis.
- Suppression of Bax and overexpression of Bcl-2 protein is an early event in gastric tumorigenesis, before gastric dysplastic changes occur.
- RASSF1A is a tumor suppressor that activates Bax via MOAP-1
- activation of the c-Abl-PKCdelta-Rac1-p38 MAPK pathway in response to ionizing radiation signals conformational changes of Bak and Bax, resulting in mitochondrial activation-mediated apoptotic cell death in human non-small cell lung cancer cells
- Helicobacter pylori vacuolating cytotoxin induces activation of the proapoptotic proteins Bax and Bak
- At the molecular level cisplatin increased P53 and BAX expression in comparison with its complex with 3-aminoflavone.
- interference with the p53/PUMA/Bax cascade is crucial for the antiapoptotic function of the viral E6 oncogene in HPV-positive cancer cells
- beta amyloid-induced neurotoxicity occurs via bax over-expression, B-cell lymphoma protein 2 down-regulation, and caspase-3 activation, first indicating that methionine 35 redox state may alter this cell death pathway
- androgen and androgen receptor promote Bax-mediated apoptosis in prostate cancer cells.
- an independent prognostic marker in stage III colrectal carcinoma
- caspase-6 and its cleavage of lamin A are critical in apoptotic signaling triggered by resveratrol in the colon carcinoma cells, which can be activated in the absence of Bax or p53
- No significant differences within the expression of Bcl-2 family member proteins in B-cell chronic leukemia.
- The expression of all X-chromosome RBM genes was significantly associated with the expression of the proapoptotic Bax gene
- BH3 has a role in apoptosis in neuroblastoma
- Taken together, these findings suggest that Bax and caspase activation, together with PKCdelta signaling are involved in c-Myc-dependent etoposide-induced apoptosis.
- the ratio of Bax:Bcl-2 in the human oviduct increases significantly in the luteal phase consistent with cells undergoing apoptosis
- ALK7-induced apoptosis is at least in part through two Smad-dependent pathways, Bax/Bcl-2 and Xiap.
- PUMA initiates apoptosis in part by dissociating Bax and Bcl-X(L), thereby promoting Bax multimerization and mitochondrial translocation
- Variations in TP53 and BAX alleles are unrelated to the development of pemphigus foliaceus.
- Data suggest that Bcl-2 functions as an inhibitor of mitochondrial permeabilization by changing conformation in the mitochondrial membrane to bind membrane-inserted Bax monomers and prevent productive oligomerization of Bax.
- Bax is phosphorylated by stress-activated JNK and/or p38 kinase and phosphorylation of Bax leads to mitochondrial translocation prior to apoptosis
- Radiation therapy for squamous cell carcinoma of cervix results in increased apoptosis with the up-regulation of Bax, a proapoptotic protein, the down-regulation of Bcl-XL, an antiapoptotic protein, and no significant change in the levels of Bcl-2.
- p21WAF1 and Bax may be used as the markers in the assessment of GIST malignant potential.
- anti-beta-2 glycoprotein I antibodies react with trophoblast cells and reduce the cell lymphoma protein 2/Bax ratio, but without any clear apoptotic effect
- In Bax(-/-)/Bak(-/-) cells a nonapoptotic pathway dependent on sustained autophagy commits the oxidatively damaged cells to death.
- The structure reveals the conformation of the 6A7 peptide epitope on Bax in the activated form and elucidates the extensive structural changes that Bax must undergo during the conversion from its native to its activated conformation.
- The high expression of bax in Hodgkin and Reed-Sternberg cells in most classical Hodgkin's lymphomas (HLs)indicates that this protein may play predominant role in the regulation of apoptosis in classical HLs.
- tBID engages BAX to trigger its pro-apoptotic activity
- inhibiting the fission machinery in Bax/Bak-mediated apoptosis, by down-regulating of Drp1 or hFis1, prevents the fragmentation of the mitochondrial network
- down-regulation of the neuropilin-1 transcripts by short interfering RNA caused spontaneous synoviocyte apoptosis, which was associated with both the decrease in Bcl-2 expression and the increase in Bax translocation to mitochondria.
- membrane targeting of stapled BID BH3 optimizes its ability to activate BAX, supporting a model in which BID directly engages BAX to trigger mitochondrial apoptosis
- Bax is likely to be the key effector of Maspin-mediated induction of apoptosis as indicated by the activation of cleaved caspase-3.
- in addition to interacting with the pro-apoptotic protein Bak, vaccinia F1L also functions to indirectly inhibit the activation of Bax, likely by interfering with the pro-apoptotic activity of BH3-only proteins such as BimL
- Survivin fused to a nuclear localization signal augmented basal expression levels of p53 and Bax and enhanced sensitivity for intrinsic apoptosis
- The expression of p53, Bcl-2 and Bax was altered in lung cancer tissue compared to histologically normal bronchial epithelium.
- Hypochlorous acid induced Bax-dependent mitochondrial permeability which led to cell death without caspase activity by processes involving AIF/EndoG-dependent pathways.
- In CD3+ cells from B-Cell chronic lymphocytic leukemia(B-CLL) patients, Bax expression was suppressed. Apoptosis inhibition in CD3+ cells suggests a pivotal role of T-cells in B-CLL pathogenesis.
- We show that Bax activation by Vpr was ablated when ATR or GADD45alpha was knocked down.
- Reviewer states that the role(s) of Bax in neuronal dysfunction and/or death may be dependent on the disease context. Future studies will determine whether Bax plays a broad role in death and dysfunction of neurons in neurodegenerative disease.
- pro-apoptotic Bax/Bcl-2 are upregulated in human leukemic HL-60 cells after treatment with ethyl acetate extract of Chinese medicinal herb Sarcandra glabra
- Bax and Bim are upregulated in human B cells during arsenic trioxide induction of apoptosis via the mitochondrial pathway
- the interaction between ETS1 and GFI1 facilitates their binding to specific sites on the Bax promoter and represses Bax expression
- Bax is required to activate effector caspases, and to accomplish DNA damage and Neisseria gonorrhoeae-induced apoptosis.
- modified LDL results in an increased transfer of mitochondria-derived superoxide anion to p53, which stimulates a conformational change in Bax favoring its translocation to the mitochondria with resultant apoptosis of progenitor cells
- Bax promotes efficient release of intermembrane space proteins through the outer membrane of yeast mitochondria while the inner membrane remains intact.
- STAT1 and TA-p73 can interact directly, and p73-mediated Bax promoter activity was observed to be reduced by STAT1 expression in a p53-independent manner for which STAT1 Tyrosine-701 and Serine-727 are key residues.
- Results indicate that both mutations and BAX protein levels are useful molecular biological markers for prognosis and clinical management of pediatric GCT.
- Lysosome is the primary target and the axis cathepsin D-Bax as the effective pathway of hydrogen peroxide lethal activity in neuroblastoma cells.
- Significant coexpression of GLUT-1, Bcl-xL, and Bax points to cooperation of all three regulatory proteins in elimination due to irreversible injury, adaptation to hypoxia, reduction of further damage, and survival of colorectal cancer cells.
- BAX protein expression may be of central significance for clinical outcome to fluorouracil based adjuvant chemotherapy in stage III colon cancer.
- BH3-only proteins and BH3 mimetics induce autophagy by competitively disrupting the interaction between BECN1 and BAX.
- Substitution of a nucleotide G-->A at position -248 in the bax gene was more frequent in patients with osteomyelitis and was associated with a longer lifespan of their peripheral blood neutrophils and lower Bax protein expression
- Two amino acids, leucine-70 and aspartate-71, within the BH3 homology domain of Bax play a critical role in regulating its multimeric state, localization and activation.
- The results show that the failure of PrP mutants to produce cytosolic PrP is responsible for the loss of anti-Bax function and that the effect of the PrP mutants is dominant over wild-type PrP.
- The amino-acid segments within Bax that are critical for Bax interaction with viral mitochondrial inhibitor of apoptosis/vMIA/UL37 complex are reported.
- These results demonstrate that BimL is involved in UV irradiation-induced apoptosis by indirectly activating Bax.
- the results of this study showed a frameshift mutation with a deletion of C base at nucleotide 153 of exon 6 of the BAX gene in a cases of a glioblastoma multiform (WHO Grade IV) sample.
- mitochondria-mediated cell death by DATS is associated with ROS generation and regulated by Bax/Bak but independent of Bcl-2 or Bcl-xL
- The analysis of Bax deletion constructs indicates that the N-terminus drives conformational changes facilitating inhibition of cytotoxicity by Bcl-xL.
- PKCzeta may function as a physiological Bax kinase to directly phosphorylate and interact with Bax, which leads to sequestration of Bax in cytoplasm and abrogation of the proapoptotic function of Bax
- The expression and subcellular localization of BAX protein in the nucleus demonstrated the involvement of this protein in the photo-oxidative cell death pathway.
- Inhibition of ubiquitin-mediated degradation of MOAP1 by apoptotic stimuli promotes BAX function in mitochondria.
- although the carboxyl terminus of Bax is not implicated in its mitochondrial localization, it has a role in the dimerization process and thus in its activity
- Bcl-2 immunohistochemical profile may be useful in detecting adenomas with a malignant potential, and in combination with Dukes stage, may predict prognosis in colorectal cancer.
- These data suggest that long-term androgen deprivation + radiotherapy should be used when either Bcl-2 or Bax is abnormally expressed.
- Low expression of Bax is associated with poor survival of patients with locally advanced esophageal cancer treated with chemoradiotherapy.
- Most Fanconi anaemia peripheral blood lymphocytes samples displayed increased levels of Bax protein and were more susceptible to both spontaneous apoptosis and mitogen activation-induced cell death.
- mitochondrial TOM complex is required for tBid/Bax-induced cytochrome c release
- Impaired kinetics of Bax-GFP and Smac/DIABLO-GFP in caspase 8 and bid-silenced and Bcl-2- overexpressed breast cancer cells exposed to camptothecin.
- These results suggest that PKCepsilon mediates its effects on TNFalpha- based apoptosis partly by preventing activation and translocation of Bax to the mitochondria.
- Alterations in TGF-betaRII, BAX, IGFIIR, caspase-5, hMSH3 and hMSH6 genes of microsatellite instability are rare in urinary bladder carcinoma and they are not associated with microsatellite instability or the presence of p53 mutations.
- TRAIL can trigger an apoptotic pathway that involves JNK-dependent activation of Bim, which in turn induces Bax-mediated permeabilization of lysosomes.
- Risk for head and neck squamous cell carcinoma may be assocated with single-nucleotide polymorphism in the promoter region.
- Bax translocation by UV irradiation is a Bid-independent event and inhibited by overexpression of Bcl-x(L).
- We conclude that alteration in the expression of proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins on surface of thyroid follicular cells may play a role in the pathogenesis of thyroid autoimmune disorders.
- AG490 enhances UCN-01-induced cytotoxicity in p53 defective cell lines by suppression of BAD phosphorylation and induction of BAX and PARP cleavage
- Report modulation of the BCL-2/BAX ratio by interferon-gamma and hypoxia in human peritoneal and adhesion fibroblasts.
- sequential phosphorylation of these serine residues might participate in the triggering of the different conformational changes associated with Bax activation during apoptosis
- In the absence of Bax and caspase activation, inhibition of the proteasome could also kill cancer cells by an alternative, non-apoptotic form of cell death.
- Levels of IAP-2 and Bax were decreased in A375 cells and HIF-1alpha was increased during hypoxia.
- Diabetic human conjunctiva, with its inflammatory and cicatricial phenomena, is a privileged target for BAX protein apoptotic cell death.
- These results suggest that 4'-demethyl-4-dehydroxy-4-seleno-phenyl-beta-peltatin-epipodophyllotoxin (CPZ)-induced apoptosis may work through a Bax-dependent pathway.
- critical involvement of p38 MAPK, PUMA, and Bax in 6-OHDA-induced apoptosis
- Translocation of Bax was essential for TIP30-induced apoptosis, whereas overexpression of the anti-apoptotic protein Bcl-xL delayed both second mitochondria-derived activator of caspases (Smac/DIABLO) release and onset of apoptosis.
- Raf-1 in beta-cells led to a striking loss of Bad phosphorylation at serine 112 and an increase in the protein levels of both Bad and Bax
- Mcl-1 degradation primes the cell for Bim and Bax activation and anoikis, which can be blocked by oncogenic signaling in metastatic cells
- silencing of PrPc facilitates the activation of proapoptotic Bax by down-regulation of Bcl-2 expression, thereby abolishing the resistance of breast cancer cells to TRAIL-induced apoptosis
- observed an increase of Bax expression in preeclamptic placentas compared to the normal full-term placentas
- IL-10 modulated the pro-apoptotic capacity of TNF-alpha in chondrocytes as shown by the decrease in caspase activities and bax/bcl-2 ratio
- findings identify RelA/NF-kappaB as a critical regulator of T-cell survival by affecting the balance of Bcl-2 family members.
- Ceramide activates p38MAPK, which inhibits Akt and leads to Bax translocation.
- These findings suggest that downregulating CIAPIN1 could sensitize leukemia cells to chemotherapeutic drugs by downregulating MDR-1 and Bcl-2 and by upregulating Bax.
- Negative Bax protein expression in tumour cells was correlated with lymph node metastasis and degree of differentiation. Negative Bax expression in gastric cancer is associated with de-differentiation, lymph node metastases, and poor clinical prognosis.
- the pro-survival activity of MCL-1 proceeds via inhibition of BAX function at mitochondria, downstream of its activation and translocation to this organelle.
- Patients bearing bax positive/cytochrome c positive tumors have a decreased 4-year disease-free survival rate compared to the rest of the group.
- Bax instability may represent a final common pathway for disparate prognostic markers, as well as being itself an indicator of poor prognosis.
- Differentiation- and apoptosis-associated changes in the pattern of Bax cellular distribution are uncovered with anti-Bax Abs and suggest Bax undergoes successive activation that progresses in parallel with keratinocyte differentiation and apoptosis.
- distinctions in the behaviors of Bcl-B and Mcl-1 relative to the other anti-apoptotic Bcl-2 family members, where Bcl-B and Mcl-1 display reciprocal abilities to bind and neutralize Bax and Bak.
- In an epigenetic aspect, both MACS and MSI+ had a high rate of CpG island methylator phenotype (46.2 and 42.9%). However, they differed in the presence of hMLH1 methylation (7.7 vs 57.1%, p < 0.05).
- BIM and tBID follow different strategies to trigger BAX-driven mitochondrial outer membrane permeabilization with strong potency
- The low frequency of apoptotic phenomena (caspase-3 and Bax) in epithelial cells of oral lichen planus may create a favourable substrate for malignant transformation.
- The present investigations demonstrate the importance of exposure of the C-terminus of Bax for its interaction with nucleophosmin. These protein-protein interaction assays provide a technical approach for the study of Bax-interacting proteins.
- Runx2-mediated activation of the Bax gene increases osteosarcoma cell sensitivity to apoptosis
- Results describe the interrelationship between H pylori and Epstein-Barr virus infection in gastric carcinogenesis, focusing on p53 mutation and c-Myc, Bcl-2 and Bax expression.
- data indicate that Bim, Bak, and Bax actively mediate osteoblast apoptosis induced by trophic factor withdrawal
- that the recruitment of YB1, PURalpha, and H1.2 to the p53 target gene Bax is required for repression of p53-induced transcription.
- Results describe, in liposomes, how phosphatidylethanolamine, cardiolipin, and its hydrolysis products affect Bax activation.
- Data show that following apoptotic stimuli, HtrA2 accumulates in the nucleus and cleaves p73alpha in the C-terminal portion, enabling the protein to increase its transactivation activity on Bax but not on the cell-cycle regulator gene p21.
- These data show that Hsp27 antagonizes Bax-mediated mitochondrial injury and apoptosis by promoting Akt activation via a PI3-kinase-dependent mechanism.
- BI-1 and Bcl-X(L) operate downstream of or parallel to Bax/Bak
- These results indicate that Bax oligomerization is an event that must be interpreted differently from the currently held view that it represents the apoptotic pore.
- The present report provides for the first time information that implicates Bax in the zinc induction of mitochondrial apoptogenesis.
- a critical role of cysteine 62 in oxidative stress-induced Bax activation and subsequent apoptosis.
- Ku70 regulates apoptosis by sequestering Bax from the mitochondria and mediating Bax deubiquitylation
- Hierarchical involvement of Bak, VDAC1 and Bax in cisplatin-induced cell death.
- Although knockdown of c-Myc or caspase-2 does not affect Bax expression, caspase-2 is important for cytosolic Bax to integrate into the outer mitochondrial membrane, and c-Myc is critical for oligomerization of Bax once integrated into the membrane
- Bax expression is reduced in airway epithelial cells of even mild asthmatic subjects and suggest that restoring Bax expression may provide a clinical approach for restoring the normal numbers of epithelial cells & reduced mucous hypersecretion in asthma.
- Bax-Delta1-66 mutant was not able to induce apoptosis;the alpha5 helix of Bax is sensitive to ubiquitin-dependent degradation.
- It is concluded that P. aeruginosa can induce apoptosis with an up-regulated expression of Bax and a down-regulated expression of Bcl-2, which resulted in increased levels of cytochrome c release and increased caspase-3 and -9 in human U937 cells.
- The distribution of the bcl-2, bax and caspase-3 proteins was investigated in the cells of developing human spinal ganglia.
- Synergistic induction of apoptosis after exposure to LBH589 and bortezomib was partially mediated by Bax translocation from the cytosol to the mitochondria resulting from Bax conformational changes
- Induction of apoptosis by a stilbene analog involves Bax translocation regulated by p38 MAPK and Akt.
- DE-71 induces the apoptosis of [Ca(2+)](i) in human neuroblastoma cells via Bax insertion, Cyt c release in the mitochondria, and the caspase activation pathway.
- Bax over-expression restored back theaflavin-induced apoptosis in pifithrin-alpha-inhibited/dominant-negative p53-expressing cells.
- Kynurenic acid attenuates MPP(+)-induced dopaminergic neuronal cell death via a Bax-mediated mitochondrial pathway.
- PKC delta in preeclamptic placentas promotes Bax dissociation from 14-3-3 zeta through 14-3-3 zeta phosphorylation.
- Prolonged hypoxia-reoxygenation caused the most severe villous apoptotic changes, increased the expression of Bax and Bak mRNA and protein and reduced the expression of Bcl-2 mRNA.
- Src phosphorylation of Bif-1 suppresses the interaction between Bif-1 and Bax, resulting in the inhibition of Bax activation during anoikis.
- HBx induces apoptosis by interacting with Bax and enhancing its translocation to mitochondria
- Higher expression of Bax in T cells, regulatory (Tregs) decreases the striking threshold of vascular inflammation due to the failure of suppression of inflammatory cells resulting from Treg apoptosis.
- Bax protein (BCL2-associated X protein) levels were significantly higher in tissue samples from subjects with emphysema (both smokers and ex-smokers)
- Strong BAX signal was detected in oogonia and oocytes from week 12 to term.
- Detail the role of Bax translocation, cytochrome c release, and perinuclear clustering of the mitochondria in the killing of HeLa cells by TNF.
- Bax mRNA therapy using cationic liposomes for melanoma is reported.
- The presence of cholesterol in membranes inhibits the pore-forming activity of BAX by reducing the ability of BAX to transition from a membrane-associated protein to a membrane-integral protein.
- cytosolic prion protein (PrP) is the predominant form of PrP with anti-Bax function
- Expressed in most dysmorphic neurons in focal cortical dysplasia type II.
- NBS1 regulates a novel p53 independent apoptotic pathway in response to DNA damage.
- mRNA expressions of Hsp70, Hsp32 and Bax significantly increased in mononuclear blood cells after marathon running, whereas Hsp27 and Bad mRNA expression levels showed no significant changes.
- These findings suggest JNK to have an important pro-apoptotic function following ultraviolet rays B irradiation in human melanocytes, by acting upstream of lysosomal membrane permeabilization and Bim phosphorylation.
- thrombin induces activation and mitochondrial translocation of Bid, Bax and Bak, and evokes mitochondrial membrane depolarization
- m38.5 associates with Bax, recruits it to mitochondria, and blocks Bax-mediated but not Bak-mediated mitochondrial outer membrane permeabilization.
- Down-regulation of either acid sphingomyelinase or LASS 5-attenuated ceramide accumulation and H/R-induced Bax translocation to mitochondria.
- The survival-promoting effect of CXCL12 was mediated by the up-regulation of Bcl-2 protein expression and the concomitant down-regulation of Bax protein expression
- cytosolic cyclin D1 is able to regulate apoptosis by interaction with Bax in LDIR-induced adaptive resistance.
- Ki-67 and bcl-2 expression was correlated with tumor grade, and the higher the tumor grade, the higher the Ki-67 and bcl-2 expression.
- expression & distribution of Bax & Bcl-2 molecules in term, pre-term & post-term placentas; Bax/Bcl-2 ratio was higher in both pre-term & post-term placental samples compared with term placentas
- Low expression of Bax was significantly associated with male gender, squamous cell histology and low expression of galectin-3 in lung cancer.
- DDA3 binds and inhibits ASPP2 in stimulating the p53-dependent BAX promoter activation without affecting the binding of ASPP2 to p53.
- combined gamma-irradiation and CI/RA treatment of the cells changed the equilibrium between Bax and Bcl-2 mRNA to anti apoptotic state with increased expression of Bcl-2 and almost abolished expression of Bax.
- Immunohistochemistry using antibodies to determine the protein expression of Fas, Fas-L, Bax, Bcl-2, p53 and c-Myc in skin of venous ulcer patients.
- Results describe the immunohistochemical distribution of caspase 3, 9 and Bax in intracranial U87 glioblastoma xenografts, and show that xenografts contain cells positive for caspase-3, caspase-9, and Bax.
- BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk
- These findings suggest that Bax mediates cytochrome c release and mitochondrial depolarization in lymphocytes, at least in part, via its interaction with mitochondrial Kv1.3.
- an intracellular wave of cytochrome c propagates and precedes Bax redistribution during apoptosis
- There was an association between BCL2 and diffuse large B-cell lymphoma: significant relationship between BCL2 expression and FOXP1 genetic abnormalities and between BCL2 expression and BCL2 genetic abnormalities.
- CK7, bax, CCND1, and HER2 represent marker proteins and frequently amplified genes in carcinomas of the ampulla of Vater.
- BIM stabilized alpha-helix of BCL-2 domains binds BAX at an interaction site that is distinct from the canonical binding groove characterized for anti-apoptotic proteins
- Bcl-xL phosphorylation induced by microtubule inhibitors plays a key pro-apoptotic role at least in part by disabling the ability of Bcl-xL to bind Bax.
- Increased level of Bax protein expression is associated with chronic myelogenous leukemia.
- This study demonstrated that baicalin-induced apoptotic cell death in the breast cancer cells involves the up-regulation of proapoptotic p53 and bax, implying potential crucial roles of bax and p53 in the baicalin-induced apoptosis.
- BAX and BAK proteins are required for cyclin-dependent kinase inhibitory drugs to cause apoptosis
- This study demonstrated that RhoE may promote the multidrug resistance phenotype of gastric cancer cells by decreasing the expression of Bax at posttranscriptional level, thus inhibiting vincristine-induced apoptosis.
- increased expression of Bif-1 in Merkel cell carcinoma is associated with low levels of Bax staining
- Baxbeta protein is ubiquitously present among human cells, but its activity is restricted through stringent regulation by proteasomal degradation.