Retinoic acid as cause of cell proliferation or cell growth inhibition depending on activation of one of two different nuclear receptors.
Retinoic acid can combine with the nuclear retinoic acid receptor (RAR), leading to cell growth inhibition, as in certain tumors. Retinoic acid can also bind to the orphan nuclear receptor peroxisome proliferator-activated receptor beta/delta (PPAR beta/delta), resulting in stimulation of cell growth and inhibition of apoptosis. To bind to RAR, retinoic acid is carried into the nucleus by the cytosolic cellular retinoic acid-binding protein-II; to bind to PPAR beta/delta, it is transported into the nucleus by the cytosolic fatty acid-binding protein 5.
Wolf
George
G
Department of Nutritional Sciences and Toxicology, University of California, Berkeley, CA, USA. nutritionreview@ilsi.org
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival; D050556:Fatty Acid-Binding Proteins / Q000235:genetics / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D047494:PPAR delta; D048068:PPAR-beta; D018168:Receptors, Retinoic Acid / Q000235:genetics / Q000378:metabolism*; D014212:Tretinoin / Q000494:pharmacology*
D000970:Antineoplastic Agents; C493412:FABP5 protein, human; D050556:Fatty Acid-Binding Proteins; D047494:PPAR delta; D048068:PPAR-beta; D018168:Receptors, Retinoic Acid; C082928:retinoic acid binding protein II, cellular; D014212:Tretinoin