S
Scott M. Kulich
Researcher at University of Pittsburgh
Publications - 17
Citations - 2465
Scott M. Kulich is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Kinase & MAPK/ERK pathway. The author has an hindex of 13, co-authored 17 publications receiving 2259 citations. Previous affiliations of Scott M. Kulich include Veterans Health Administration.
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Journal ArticleDOI
Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission
Ruben K. Dagda,Salvatore J. Cherra,Scott M. Kulich,Scott M. Kulich,Anurag Tandon,David S. Park,Charleen T. Chu +6 more
TL;DR: It is found that loss of PINK1 function elicits oxidative stress and mitochondrial turnover coordinated by the autophagic and fission/fusion machineries, and Pink1 and Parkin may cooperate through different mechanisms to maintain mitochondrial homeostasis.
Journal ArticleDOI
Regulation of the autophagy protein LC3 by phosphorylation
Salvatore J. Cherra,Scott M. Kulich,Scott M. Kulich,Guy Uechi,Manimalha Balasubramani,John Mountzouris,Billy W. Day,Charleen T. Chu +7 more
TL;DR: PKA puts the brakes on autophagy by inhibiting LC3 recruitment to autophagosomes in mice and spares the cell from apoptosis.
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Oxidative neuronal injury: The dark side of ERK1/2
Charleen T. Chu,David J. Levinthal,Scott M. Kulich,Elisabeth M. Chalovich,Donald B. DeFranco +4 more
TL;DR: It is proposed that differential accessibility of ERK1/2 to downstream targets, which is dictated by the persistent activation of ERk1/1 within distinct subcellular compartments, underlies the neurotoxic responses that are driven by this kinase.
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Mitochondrially localized ERK2 regulates mitophagy and autophagic cell stress: implications for Parkinson's disease.
TL;DR: It is shown that 6-hydroxydopamine elicits activity-related localization of ERK1/2 in mitochondria of SH-SY5Y cells, and these events coincide with induction of autophagy and precede mitochondrial degradation, indicating that mitochondrial localization ofERK2 activity is sufficient to recapitulate the effects of 6-OHDA on mitophagyand autophagic cell death.
Journal ArticleDOI
Sustained Extracellular Signal-Regulated Kinase Activation by 6-hydroxydopamine: Implications for Parkinson's Disease
Scott M. Kulich,Charleen T. Chu +1 more
TL;DR: The results suggest that ERKactivation plays a direct mechanistic role in 6‐OHDA toxicity, rather than representing a protective compensatory response, and raise the possibility that abnormal patterns of ERK activation may contribute to dopaminergic neuronal cell death.