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Cell Biology Commons

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2014

Australian Catholic University

Articles 1 - 2 of 2

Full-Text Articles in Cell Biology

Structural Basis For Phosphorylation And Lysine Acetylation Cross-Talk In A Kinase Motif Associated With Myocardial Ischemia And Cardioprotection, Benjamin L. Parker, Nicholas E. Shepherd, Sophie Trefely, Nolan John Hoffman, Melanie Y. White, Kasper Engholm-Keller, Brett D. Hambly, Martin R. Larsen, David E. James, Stuart J. Cordwell Jan 2014

Structural Basis For Phosphorylation And Lysine Acetylation Cross-Talk In A Kinase Motif Associated With Myocardial Ischemia And Cardioprotection, Benjamin L. Parker, Nicholas E. Shepherd, Sophie Trefely, Nolan John Hoffman, Melanie Y. White, Kasper Engholm-Keller, Brett D. Hambly, Martin R. Larsen, David E. James, Stuart J. Cordwell

Faculty of Health Sciences Publications

Myocardial ischemia and cardioprotection by ischemic pre-conditioning induce signal networks aimed at survival or cell death if the ischemic period is prolonged. These pathways are mediated by protein post-translational modifications that are hypothesized to cross-talk with and regulate each other. Phosphopeptides and lysine-acetylated peptides were quantified in isolated rat hearts subjected to ischemia or ischemic pre-conditioning, with and without splitomicin inhibition of lysine deacetylation. We show lysine acetylation (acetyl-Lys)-dependent activation of AMP-activated protein kinase, AKT, and PKA kinases during ischemia. Phosphorylation and acetyl-Lys sites mapped onto tertiary structures were proximal in >50% of proteins investigated, yet they were mutually ...


Mutant Tdp-43 Deregulates Ampk Activation By Pp2a In Als Models, Nirma Perera, Rebecca Sheean, John Scott, Bruce Kemp, Malcolm Horne, Bradley Turner Jan 2014

Mutant Tdp-43 Deregulates Ampk Activation By Pp2a In Als Models, Nirma Perera, Rebecca Sheean, John Scott, Bruce Kemp, Malcolm Horne, Bradley Turner

Faculty of Health Sciences Publications

Bioenergetic abnormalities and metabolic dysfunction occur in amyotrophic lateral sclerosis (ALS) patients and genetic mouse models. However, whether metabolic dysfunction occurs early in ALS pathophysiology linked to different ALS genes remains unclear. Here, we investigated AMP-activated protein kinase (AMPK) activation, which is a key enzyme induced by energy depletion and metabolic stress, in neuronal cells and mouse models expressing mutant superoxide dismutase 1 (SOD1) or TAR DNA binding protein 43 (TDP-43) linked to ALS. AMPK phosphorylation was sharply increased in spinal cords of transgenic SOD1G93A mice at disease onset and accumulated in cytoplasmic granules in motor neurons, but not in ...