Human Apoptosis regulator BAX ELISA Kit

Code CSB-E09344h
Size 96T,5×96T,10×96T
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Product Details

Target Name
BCL2-associated X protein
Alternative Names
Apoptosis regulator BAX ELISA Kit; BAX ELISA Kit; Bax-protein ELISA Kit; BAX_HUMAN ELISA Kit; BAXA ELISA Kit; Baxdelta2G9 ELISA Kit; Baxdelta2G9omega ELISA Kit; Baxdelta2omega ELISA Kit; Bcl-2-like protein 4 ELISA Kit; BCL2 associated X protein ELISA Kit; BCL2 associated X protein omega ELISA Kit; BCL2 associated X protein transcript variant delta2 ELISA Kit; Bcl2-L-4 ELISA Kit; BCL2L4 ELISA Kit; membrane isoform alpha ELISA Kit
Uniprot No.
Homo sapiens (Human)
Sample Types
serum, plasma, tissue homogenates
Detection Range
1.25 ng/mL-80 ng/mL
0.312 ng/mL
Assay Time
Sample Volume
Detection Wavelength
450 nm
Research Area
Cell Biology
Assay Principle
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
To assess the linearity of the assay, samples were spiked with high concentrations of human BAX in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
1:1Average %95
Range %87-101
1:2Average %94
Range %91-103
1:4Average %95
Range %92-100
1:8Average %94
Range %88-97
The recovery of human BAX spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample TypeAverage % RecoveryRange
Serum (n=5) 10296-109
EDTA plasma (n=4)9690-100
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
802.305 2.215 2.260 2.108
401.675 1.765 1.720 1.568
201.164 1.172 1.168 1.016
100.795 0.809 0.802 0.650
50.453 0.447 0.450 0.298
2.50.322 0.336 0.329 0.177
1.250.225 0.219 0.222 0.070
00.152 0.151 0.152  
and FAQs
Store at 2-8°C. Please refer to protocol.
Lead Time
3-5 working days after you place the order, and it takes another 3-5 days for delivery via DHL or FedEx

The human BAX ELISA kit (CSB-E09344h) is designed for the quantitative measurement of human BAX protein in serum, plasma, or tissue homogenates. It quantitates human BAX with 0.312 ng/ml sensitivity and shows excellent specificity for human BAX. It uses the bi-antibody sandwich enzyme immunoassay technique. This assay employs a biotin-conjugated BAX antibody that recognizes the analyte bound by the immobilized BAX antibody, forming an antibody-analyte-antibody complex. The immune complex is further detected by avidin-conjugated HRP. The TMB solution is added into the wells and turns blue and finally turns yellow after the addition of the stop solution. Solution color develops in proportion to the amount of BAX in the sample. The O.D. value is measured using a microplate reader at 450 nm and is used to determine the concentration of the human BAX in the sample.

BAX is one of the pro-apoptotic proteins of the BCL2 gene family that mediates mitochondrial fusion. BAX is essential for mitochondrial fusion in healthy cells. During apoptosis, BAX is recruited and oligomerized at mitochondrial foci. BAX is involved in the formation of pores that enables the mitochondrion to cytochrome c and subsequent activation of caspase cascade release, finally leading to apoptosis.

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Target Background

(From Uniprot)
Plays a role in the mitochondrial apoptotic process. Under normal conditions, BAX is largely cytosolic via constant retrotranslocation from mitochondria to the cytosol mediated by BCL2L1/Bcl-xL, which avoids accumulation of toxic BAX levels at the mitochondrial outer membrane (MOM). Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis.
Gene References into Functions
  1. 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) PMID: 29233735
  2. 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. PMID: 29767244
  3. 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. PMID: 29750299
  4. 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. PMID: 28368610
  5. 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 PMID: 28933587
  6. There is no significant association between BAX gene polymorphism and cancer susceptibility, but it probably contributes to increased adverse prognosis to cancer. PMID: 30024563
  7. 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. PMID: 29207051
  8. 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. PMID: 28795366
  9. helix alpha9 assists Bax activation via the dimer heterogeneity and interactions with specific MOM lipids, which eventually facilitate proteolipidic pore formation in apoptosis regulation PMID: 27381287
  10. 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. PMID: 27620692
  11. 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 PMID: 28438509
  12. 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 PMID: 27630059
  13. 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) PMID: 29246973
  14. High expression of BAX is associated with colorectal cancer. PMID: 28586030
  15. High mitochondrial Bax apoptosis regulator protein (BAX) levels correlate with improved acute myeloid leukemia (AML) patient survival. PMID: 28420723
  16. parkin-dependent targeting of misregulated BAX on the mitochondria provides substantial protection against BAX apoptotic activity. PMID: 28760928
  17. 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. PMID: 27098707
  18. SFRP5 confers protection against oxidative stress-induced apoptosis through inhibition of beta-catenin activation and downregulation of Bax. PMID: 28834606
  19. The ratio of Bax/Bcl-2 was significantly enhanced by the Ginsenoside Rg3 to Paclitaxel. PMID: 28231544
  20. this study show that PATZ1 expression correlates positively with BAX and negatively with BCL6 and survival in human diffuse large B cell lymphomas PMID: 27494852
  21. YY1 promotes apoptosis via upregulating Bax transcription and subsequent activation of Bax by translocation from the cytosol to the mitochondrial membrane. PMID: 27074573
  22. Immunohistochemical analysis showed that STAT3, GRP78 and BAX protein levels in the combination group were significantly higher than those in STAT3 group and CDDP group (P<0.05). Exogenous STAT3 and CDDP may synergistically inhibit the xenograft tumour growth through up-regulation of BAX protein via GRP78. PMID: 27129294
  23. This is the first study evaluating the potential relationship between BCL2 and BAX gene polymorphisms and RRD in a Greek population, showing a significant association between BAX rs4645878 polymorphism and RRD susceptibility. This finding suggests that an apoptotic mechanism is implicated in the pathogenesis of RRD PMID: 28877516
  24. Heavy ion irradiation could induce p53(-/-) hepatoma cells to undergo apoptosis via E2F1/Bax/Casp3 signaling pathway. PMID: 28500630
  25. Bax effects were dependent on its oligomeric state. Monomeric Bax did not affect the membrane, oligomeric Bax lowered the breakthrough force of the membrane, which in the context of pore formation, implies a lowering of the line tension at the edge of the pore. PMID: 27755971
  26. The C-terminal helical conformation of Bax, not its primary sequence, appears to be critical for CASP8 recruitment and activation culminating in cell death. PMID: 28807790
  27. An autoinhibited dimeric form of BAX regulates the cytosolic BAX activation pathway. PMID: 27425408
  28. Although TP53 and BAX immunoreactivity levels were associated with some clinicopathological parameters of the patients, the expression of EP300, TP53 and BAX did not reveal any prognostic significance in ccRCC PMID: 28551630
  29. Cells expressing mitoCERT import ceramides into mitochondria and undergo Bax-dependent apoptosis. PMID: 27888218
  30. Results support the hypothesis that the mitochondrion-specific lipid cardiolipin functions as a first contact site for Bax during its translocation to the mitochondrial outer membrane in the onset of apoptosis. In addition, dye leakage assays revealed that different oxidized phospholipids species in the mitochondrial outer membrane-mimicking vesicles can have opposing effects on Bax pore formation. PMID: 28538152
  31. The substitution of proline 168 for alanine favors Bax oligomerization. PMID: 28322731
  32. Data show that the increased acetylation of Ku autoantigen 70kDa (Ku70) in sirtuin 6 protein (SIRT6)-depleted cells disrupt its interaction with Bax apoptosis regulator protein (Bax), which finally resulted in Bax mitochondrial translocalization. PMID: 28238784
  33. Rhaponticum carthamoides extracts from transformed and normal roots increased the ratio of Bax/Bcl-2 proteins and increased TP53 levels to reduce glioma cell proliferation. PMID: 27696406
  34. these results indicate that EVA71 infection directly impacts the mitochondrial apoptotic pathway by modulating the recruitment and activation of Bax. PMID: 28073399
  35. the present study demonstrated that DAPK contributed to the Hcyinduced endothelial apoptosis via modulation of Bcl2/Bax expression levels and activation of caspase 3 PMID: 27633052
  36. The present study evaluates the prognostic role of the p53, Bax, Bcl-2 and cyclin E immunoexpression in colon cancer. PMID: 27151692
  37. The high expression of the BAX gene seems to be a negative regulator of autophagy in colorectal cancer cells. The relative downregulation of autophagy-related genes was observed in colorectal cancer samples. PMID: 28035578
  38. High expression of BAX is associated with hepatocellular carcinoma. PMID: 27699664
  39. Low BAX/BCL2 mRNA is associated with laryngeal squamous cell carcinoma. PMID: 27129795
  40. It was concluded that ginsenoside Rh2-O induced apoptosis of HepG2 cells through activation of the lysosomal-mitochondrial apoptotic pathway involving the translocation of Bax to the lysosome. PMID: 27120618
  41. Findings reveal a novel mechanism by which p53 utilizes TFIIS.h to selectively promote the transcriptional elongation of the bax gene, upsurging cell death in response to severe DNA damage. PMID: 27005522
  42. elevated MMP-2 expression and disturbance balance of Bcl-2/BAX expressions may be associated with the development and maintenance of atrial fibrillation. PMID: 27141955
  43. TG2 can inhibit tumor cell apoptosis through down-regulation of Bax and prevention of release Cyt C from mitochondria into cytoplasm PMID: 25561282
  44. Bcl-2 and Bax expression was significantly associated with histologic grade and clinical stage, which are classic factors of poor prognosis. We suggest the use of these proteins as potential prognostic markers in STS of extremities PMID: 25906122
  45. The aim of this study was to determine the expression of apoptotic factors Bax, Bcl-2, and Caspase-3 in lens epithelial cells (LECs) from cataracts secondary to pars plana vitrectomy with silicone oil (SO) tamponade. PMID: 26956740
  46. The expression of PHF20 was associated with Bax expression. PMID: 26722404
  47. Deletion of chromosomal region 19q13.1-13.4 is common in hereditary non-polyposis colorectal cancer (CRC). This deletion could be the cause of the reduction in the expression of the BAX gene observed in CRC. PMID: 26228962
  48. miR-449 regulates the SIRT1/p53/BAX pathway, which may be its possible mechanism in modulating cell apoptosis of cisplatin-induced Acute kidney injury. PMID: 26968221
  49. Polymorphism of BAX and TP53 genes may be potential genetic modifiers for developing ovarian cancer. PMID: 26209050
  50. BimEL-Bax pro-apoptotic cascade is activated by cAMP signalling of Bordetella adenylate cyclase toxin through SHP-1 phosphatase in phagocytes. PMID: 26334669

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Subcellular Location
[Isoform Alpha]: Mitochondrion outer membrane; Single-pass membrane protein. Cytoplasm.; [Isoform Beta]: Cytoplasm.; [Isoform Gamma]: Cytoplasm.; [Isoform Delta]: Cytoplasm.
Protein Families
Bcl-2 family
Tissue Specificity
Expressed in a wide variety of tissues. Isoform Psi is found in glial tumors. Isoform Alpha is expressed in spleen, breast, ovary, testis, colon and brain, and at low levels in skin and lung. Isoform Sigma is expressed in spleen, breast, ovary, testis, lu
Database Links

HGNC: 959

OMIM: 600040

KEGG: hsa:581

STRING: 9606.ENSP00000293288

UniGene: Hs.624291

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