Bax
Bax (BCL2 associated X, apoptosis regulator, also known as BCL2L4) is a pro-apoptotic member of the Bcl-2 family. It acts in the mitochondrial apoptotic process, where its translocation to the mitochondrial outer membrane leads to cytochrome c release. Browse Assay Genie's current range of Bax research reagents below, or read on for the biology behind the target.
Bax plays a central role in the mitochondrial apoptotic process. Under normal conditions the protein is largely cytosolic, because Bcl-xL (BCL2L1) mediates its constant retrotranslocation from mitochondria to the cytosol. This avoids the accumulation of toxic Bax levels at the mitochondrial outer membrane. Under stress conditions, Bax undergoes a conformational change and translocates to the mitochondrial membrane, leading to the release of cytochrome c, which in turn triggers apoptosis. Bax also promotes activation of caspase-3 (CASP3), and thereby apoptosis.
Bax belongs to the Bcl-2 family, whose members form hetero- or homodimers and act as anti- or pro-apoptotic regulators in a wide variety of cellular activities. Bax forms a heterodimer with Bcl-2 and functions as an apoptotic activator. The association and the ratio of Bax to Bcl-2 helps determine whether a cell survives or dies following an apoptotic stimulus. Bax is also reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to loss of membrane potential and cytochrome c release. UniProt lists the protein at the mitochondrial outer membrane, in the cytoplasm and in the nucleus.
The BAX gene is regulated by the tumour suppressor P53 and is involved in P53-mediated apoptosis. Multiple alternatively spliced transcript variants encoding different isoforms have been reported. Previous names include BCL2-associated X protein and the symbol BCL2L4, and mouse and rat each have a Bax ortholog.
Bax drives the mitochondrial apoptotic process, making it a core readout for studies of cytochrome c release and caspase-3 activation.
The Bax to Bcl-2 ratio helps determine cell survival or death after an apoptotic stimulus, so it is widely examined in family-wide studies.
Bax expression is regulated by P53 and contributes to P53-mediated apoptosis, linking it to tumour suppressor pathway research.
Bax translocation, Bcl-xL-mediated retrotranslocation and VDAC opening make it a model for studying mitochondrial outer membrane permeabilisation.
Bax is a pro-apoptotic Bcl-2 family protein. Under stress it changes conformation and moves to the mitochondrial outer membrane, which leads to cytochrome c release and apoptosis. It also promotes activation of caspase-3. In healthy cells it is mostly kept cytosolic by Bcl-xL.
The HGNC symbol is BAX, with BCL2L4 as an alias. Earlier names include BCL2-associated X protein, and UniProt calls it apoptosis regulator BAX. NCBI Gene reports multiple alternatively spliced transcript variants that encode different isoforms.
Mouse and rat both have a Bax ortholog; check the datasheet of any product for its validated reactivity. Bax expression is regulated by the tumour suppressor P53, and the protein is involved in P53-mediated apoptosis.
Other Bcl-2 family members, caspases and apoptosis pathway partners with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q07812; product specifications from Assay Genie datasheets.