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Studies of the functions of members of the Bcl2 gene family suggested that apoptosis was controlled by a rheostat in which anti-apoptotic proteins like BCL2 bound and sequestered pro-apoptotic proteins like BAX. Our current understanding of these proteins suggests that this is a simplistic model. The new rheostat model predicts that BH3-only peptides act as neutralizing ligands for the anti-apoptotic proteins, thus allowing molecules like BAX to become activated and initiate mitochondrial dysfunction - a critical step in the intrinsic apoptotic program. Studies of retinal ganglion cell apoptosis indicate that a threshold of BAX expression is required for its successful activation, which is independent of the overall concentration of anti-apoptotic proteins in these cells.
Department of Ophthalmology and Visual Sciences, University of Wisconsin, 1300 University Ave, Madison, WI 53706, USA. nickells@wisc.edu
11.8 Neuroprotection (Part of: 11 Medical treatment)
3.6 Cellular biology (Part of: 3 Laboratory methods)