BAX (bcl-2-like protein 4, BCL2 associated X protein) is a pro-apoptotic cytosolic protein of the Bcl-2 family that is regulated by TP53 and functions in TP53-mediated apoptosis. It changes conformation and translocates to the mitochondria following apoptotic stimuli. It is thought to share significant functional homology with Bak, another pro-apoptotic Bcl-2 family member. Disruption of BAX or Bak has little effect on cell death, but mice lacking both genes display multiple developmental defects and cells lacking both show decreased apoptotic capability. In glioma, low expression of BAX is indicative of poor prognosis. In Alzheimer’s disease, BAX is upregulated by amyloid beta peptide in neurons in the afflicted brain and is thought to contribute to neuronal cell death. Furthermore, inhibiting BAX has been found to prevent neuronal cell death induced by oligomeric amyloid beta-peptide in Alzheimer’s disease, and may be a potential therapy for the disease. In immunohistochemistry of normal tissue, BAX has moderate to high cytoplasmic positivity in most tissues throughout the body. References: J Neuropathol Exp Neurol. 1997 Jan;56(1):86-93, PMID: 8990132; J Neurosci. 1996 Dec 1;16(23):7533-9, PMID: 8922409; Cell Death Dis. 2012 May 17;3:e309, PMID: 22592316; J Neurooncol. 2019 Jan;141(1):71-81, PMID: 30446901