Aspartic acid substitutions in monoamine oxidase-A reveal both catalytic-dependent and -independent influences on cell viability and proliferation

• Published in: Journal of Neural Transmission Vol. 119; no. 11; pp. 1285 - 1294
• Main Authors: Wei, Zelan, Satram-Maharaj, Tamara, Chaharyn, Bradley, Kuski, Kelly, Pennington, Paul R., Cao, Xia, Chlan, Jennifer, Mousseau, Darrell D.
• Format: Journal Article
• Language: English
• Published: Vienna Springer Vienna 01.11.2012; Springer Nature B.V
• Subjects: Analysis of Variance; Animals; Aspartic Acid - metabolism; Basic Neurosciences; bcl-X Protein - metabolism; Bromodeoxyuridine - metabolism; Calcium - pharmacology; Catalysis - drug effects; Cell Line, Transformed; Cell Line, Tumor; Cell Proliferation - drug effects; Cell Survival - drug effects; Cell Survival - genetics; Enzyme Inhibitors - pharmacology; Genetics and Immunology - Original Article; Humans; Imidazoles - pharmacology; Immunoprecipitation; Indexing in process; Medicine; Medicine & Public Health; Mice; Monoamine Oxidase - genetics; Monoamine Oxidase - metabolism; Mutagenesis, Site-Directed - methods; Mutation - genetics; Neuroblastoma - pathology; Neurology; Neurosciences; Oxidative Stress - drug effects; Oxidative Stress - genetics; Proto-Oncogene Proteins c-bcl-2 - metabolism; Psychiatry; Pyridines - pharmacology; Serotonin - pharmacokinetics; Signal Transduction - drug effects; Signal Transduction - genetics; Superoxide Dismutase - metabolism; Superoxide Dismutase-1; Transfection; Tritium - pharmacokinetics; p38 MAP kinase; Monoamine oxidase; p42/44; Alzheimer’s disease; Catalytic dead; Akt; Proliferation; Parkinson’s disease; Cancer

Post-translational influences could underlie the ambiguous roles of monoamine oxidase-A (MAO-A) in pathologies such as depression, cancer and Alzheimer disease. In support of this, we recently demonstrated that the Ca 2+ -sensitive component of MAO-A catalytic activity is inhibited by a pro-survival...