ABMIUM target intelligence
BCL2 antagonist/killer 1
BCL2 antagonist/killer 1 (BAK1/BAK) is a pro-apoptotic BCL2-family effector located at the mitochondrial outer membrane. Following apoptotic activation, BAK changes conformation and oligomerizes to drive mitochondrial outer-membrane permeabilization. This page groups ABMIUM catalogue reagents for intrinsic-apoptosis research.
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Research context & evidence
Target information is kept separate from product-level validation so you can review the biology and the reagent evidence independently.
BAK1 is a mitochondrial apoptosis effector. Pro-apoptotic activation promotes BAK conformational change and homo-oligomerization in the outer mitochondrial membrane, increasing membrane permeability and enabling release of cytochrome c and other apoptogenic factors that support downstream caspase activation.
BAK1 is studied in intrinsic apoptosis, mitochondrial priming, BCL2-family regulation and stress-induced cell death. Experimental readouts can include BAK abundance or activation state, conformational change, oligomerization, mitochondrial cytochrome c release and downstream apoptotic signalling.
Names used across publications, databases and supplier catalogues.
