Apoptosis regulator BAX; BAX; Bax-protein; BAX; BAXA; Baxdelta2G9; Baxdelta2G9omega; Baxdelta2omega; Bcl-2-like protein 4; BCL2 associated X protein; BCL2 associated X protein omega; BCL2 associated X protein transcript variant delta2; Bcl2-L-4; BCL2L4; membrane isoform alpha

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

IgG

Rabbit

Affinity Purification

PBS with 0.02% sodium azide, 100 mug/ml BSA and 50% glycerol.

1.2 mg/mL (lot specific)

Store at -20 degree C. Avoid freeze/thaw cycles.

Manufactured in an ISO 9001:2015 Certified Laboratory.

Small volumes of anti-BAX antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

BAX, also named as BCL2L4, is a pro-apoptotic member of the Bcl-2 protein family, which plays a pivotal role in controlling cell life and death. Bax largely localizes to the cytoplasm of healthy cells, but accumulates on the outer mitochondrial membrane upon apoptosis induction. BAX can commit a cell to apoptosis by translocation from the cytosol to the mitochondria and permeabilization of the outer mitochondrial membrane, which leads to the release of cytochrome c from mitochondria. The expression of BAX is upregulated by the tumor suppressor protein p53, and BAX has been shown to be involved in p53-mediated apoptosis.

Cancer; Cell Biology; Metabolism

Western Blot (WB)

WB: 1:1000

Western Blot analysis of various samples using BAX Polyclonal Antibody at dilution of 1:1000.

Calculated: 21kDa
Observed: 21kDa

vascular endothelial growth factor A

vascular endothelial growth factor A

Apoptosis regulator BAX

BCL2L4; Bcl2-L-4??[Similar Products]

This gene is a member of the PDGF/VEGF growth factor family. It encodes a heparin-binding protein, which exists as a disulfide-linked homodimer. This growth factor induces proliferation and migration of vascular endothelial cells, and is essential for both physiological and pathological angiogenesis. Disruption of this gene in mice resulted in abnormal embryonic blood vessel formation. This gene is upregulated in many known tumors and its expression is correlated with tumor stage and progression. Elevated levels of this protein are found in patients with POEMS syndrome, also known as Crow-Fukase syndrome. Allelic variants of this gene have been associated with microvascular complications of diabetes 1 (MVCD1) and atherosclerosis. Alternatively spliced transcript variants encoding different isoforms have been described. There is also evidence for alternative translation initiation from upstream non-AUG (CUG) codons resulting in additional isoforms. A recent study showed that a C-terminally extended isoform is produced by use of an alternative in-frame translation termination codon via a stop codon readthrough mechanism, and that this isoform is antiangiogenic. Expression of some isoforms derived from the AUG start codon is regulated by a small upstream open reading frame, which is located within an internal ribosome entry site. [provided by RefSeq, Nov 2015]

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) (PubMed:21458670). 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.

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