Mark V. Stevens
National Institutes of Health
14 Papers
68 Citations
Mark V. Stevens is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Mesenchyme & Mitochondrial permeability transition pore. The author has an hindex of 12, co-authored 14 publications. Previous affiliations of Mark V. Stevens include University of Arizona.
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Papers
CD44 Attenuates Metastatic Invasion during Breast Cancer Progression
Jose Lopez,Todd D. Camenisch,Mark V. Stevens,Barbara Sands,John W. Mcdonald,John W. Mcdonald,Joyce A. Schroeder +6 more
TL;DR: Data show that during breast cancer progression, hyaluronan-CD44 dynamics occurring through epithelial-stromal interactions are protective against metastasis.
Parkin is a lipid-responsive regulator of fat uptake in mice and mutant human cells
Kye-Young Kim,Mark V. Stevens,M. Hasina Akter,Sarah E. Rusk,Robert J. Huang,Alexandra O. Cohen,Audrey Noguchi,Danielle A. Springer,Alexander V. Bocharov,Tomas L. Eggerman,Der-Fen Suen,Richard J. Youle,Marcelo Amar,Alan T. Remaley,Michael N. Sack +14 more
TL;DR: Results demonstrate that Parkin is regulated in a lipid-dependent manner and modulates systemic fat uptake via ubiquitin ligase-dependent effects and contributes to premature Parkinsonism.
Cysteine 203 of cyclophilin D is critical for cyclophilin D activation of the mitochondrial permeability transition pore.
Tiffany Nguyen,Mark V. Stevens,Mark J. Kohr,Mark J. Kohr,Charles Steenbergen,Michael N. Sack,Elizabeth Murphy +6 more
TL;DR: The results indicate that the Cys-203 residue of CypD is necessary for redox stress-induced activation of mPTP.
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MAP3Ks as central regulators of cell fate during development.
TL;DR: It is revealed that some of these MAP3K effectors may have redundant functions, and also serve as unique nexus depending on the context of the signaling pathway, which represents critical effectors that regulate extracellular stimuli into cellular responses, such as differentiation, proliferation, and apoptosis.
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Restricted mitochondrial protein acetylation initiates mitochondrial autophagy
Bradley R. Webster,Iain Scott,Kim Han,Jian H. Li,Zhongping Lu,Mark V. Stevens,Daniela Malide,Yong Chen,Leigh Samsel,Patricia S. Connelly,Mathew P. Daniels,J. Philip McCoy,Christian A. Combs,Marjan Gucek,Michael N. Sack +14 more
TL;DR: It is suggested that deacetylation of mitochondrial proteins initiates mitochondrial Autophagy in a canonical autophagy-mediator-dependent program and shows that modulation of this regulatory program has ameliorative mitochondrial homeostatic effects.
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