BAK1
BAK1 (BCL2 antagonist/killer 1, also known as BAK, BCL2L7 and CDN1) is a pro-apoptotic member of the BCL2 family that sits in the mitochondrial outer membrane. It drives the mitochondrial apoptotic process by permeabilising the membrane and releasing cytochrome c. Browse Assay Genie's current range of BAK1 research reagents below, or read on for the biology behind the target.
BAK1 plays a central role in the mitochondrial apoptotic process. When cell death signals arrive, the BAK1 protein promotes mitochondrial outer membrane (MOM) permeabilisation by oligomerising to form pores within the MOM. These pores release apoptogenic factors into the cytosol, including cytochrome c, which promotes activation of caspase 9. Caspase 9 in turn processes and activates the effector caspases that carry out cell death.
The BAK1 gene encodes a member of the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act as anti- or pro-apoptotic regulators involved in a wide variety of cellular activities. BAK1 localises to mitochondria, specifically the outer membrane, and functions to induce apoptosis. It interacts with the mitochondrial voltage-dependent anion channel and accelerates its opening, which leads to a loss of membrane potential and the release of cytochrome c. The protein also interacts with the tumour suppressor P53 after exposure to cell stress.
The gene is also listed under the aliases BCL2L7, BAK and CDN1, and its previous HGNC name was BCL2-antagonist/killer 1. The mouse ortholog is Bak1. Because BAK1 acts at the point where upstream death signals are converted into mitochondrial permeabilisation, it is a common focus for studies of apoptosis regulation and the balance between pro- and anti-apoptotic BCL2 proteins.
BAK1 oligomerises to form pores in the mitochondrial outer membrane, releasing cytochrome c and other apoptogenic factors into the cytosol.
Release of cytochrome c through BAK1 pores promotes caspase 9 activation, which then processes and activates the effector caspases.
BAK1 belongs to a family of anti- and pro-apoptotic regulators that form oligomers or heterodimers, making it central to studies of their balance.
BAK1 interacts with the tumour suppressor P53 after exposure to cell stress, linking stress responses to apoptosis.
BAK1 promotes the mitochondrial apoptotic process. On receiving cell death signals it oligomerises to form pores in the mitochondrial outer membrane, releasing cytochrome c into the cytosol. This promotes caspase 9 activation, which then activates the effector caspases.
BAK1 is also called BAK, BCL2L7 and CDN1. The HGNC full name is BCL2 antagonist/killer 1, previously written BCL2-antagonist/killer 1, and UniProt names the protein Bcl-2 homologous antagonist/killer. These names all refer to the same BCL2 family gene and protein.
A mouse ortholog, Bak1, is recorded. BAK1 interacts with the mitochondrial voltage-dependent anion channel, accelerating its opening, and with the tumour suppressor P53 after cell stress. Check the datasheet of any product for its validated reactivity.
Other BCL2 family members, caspases and apoptosis pathway partners with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q16611; product specifications from Assay Genie datasheets.