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BCL2 — GAPDH

Text-mined interactions from Literome

Tatton et al., Eur J Ophthalmol 1999 (Glaucoma...) : Mediated by GAPDH binding, DES increases mitochondrial BCL-2 and BCL-xL levels and decreases BAX levels thereby preventing the permeability transition pore (PTP) form opening and preventing apoptotic degradation
Dastoor et al., J Cell Sci 2001 : Bcl2 overexpression prevents nuclear translocation of GAPDH and apoptosis in untransfected cells, but not in transfected cells that overexpress GAPDH-GFP
Maruyama et al., J Neurochem 2001 (Parkinson Disease) : Transfection enforced Bcl-2 overexpression and an anti-Parkinson drug, rasagiline, prevent nuclear accumulation of glyceraldehyde-3-phosphate dehydrogenase induced by an endogenous dopaminergic neurotoxin, N-methyl ( R ) salsolinol
Jacquin et al., Cell Death Differ 2013 : The GAPDH dependent Bcl-xL overexpression is able to protect a subset of mitochondria from permeabilization that are required for cellular survival from CICD ... Thus, our work suggests that GAPDH overexpression could induce Bcl-xL overexpression and protect cells from CICD induced chemotherapy through preservation of intact mitochondria that may facilitate tumor survival and chemotherapeutic resistance