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Megan Mitsak

Researcher at Johns Hopkins University

Publications -  7
Citations -  522

Megan Mitsak is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Adenylyl cyclase & Phosphorylation. The author has an hindex of 6, co-authored 7 publications receiving 479 citations.

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Activation of the endoplasmic reticulum stress response in autoimmune myositis: Potential role in muscle fiber damage and dysfunction

TL;DR: Investigating the pathways of endoplasmic reticulum stress response, the unfolded protein response, and the ER overload response in muscle tissue of human myositis patients and in the mouse model indicates that the ER stress response may be a major nonimmune mechanism responsible for skeletal muscle damage and dysfunction in autoimmune myositIS.
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Ca2+-stimulated Basal Adenylyl Cyclase Activity Localization in Membrane Lipid Microdomains of Cardiac Sinoatrial Nodal Pacemaker Cells

TL;DR: It is shown by quantitative reverse transcriptase PCR that SANC express Ca2+-activated AC isoforms 1 and 8, in addition to AC type 2, 5, and 6 transcripts, and that ACs localize to membrane lipid microdomains.
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Endothelial cell activation and neovascularization are prominent in dermatomyositis

TL;DR: Gene expression analysis demonstrated that genes that participate not only in angiogenesis but also in leukocyte trafficking and the complement cascade were highly up regulated in DM muscle in comparison to age matched controls.
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Two-dimensional gel-based approaches for the assessment of N-Linked and O-GlcNAc glycosylation in human and simian immunodeficiency viruses.

TL;DR: This approach will permit correlation of virus glycosylation status with pathological severity and may serve as a rapid screen of viruses from physiological samples for further study by more advanced MS methodology.
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Altered myofilament stoichiometry in response to heart failure in a cardioprotective α-myosin heavy chain transgenic rabbit model.

TL;DR: The impact of α‐MHC overexpression on global cardiac protein expression is investigated and cardioprotective against tachycardia‐induced cardiomyopathy and mitochondrial energetics protein complement is investigated.