M
Mark E. Anderson
Researcher at Johns Hopkins University School of Medicine
Publications - 307
Citations - 20458
Mark E. Anderson is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Medicine. The author has an hindex of 72, co-authored 252 publications receiving 17510 citations. Previous affiliations of Mark E. Anderson include Vanderbilt University & University of Colorado Denver.
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Journal ArticleDOI
EH Domain Proteins Regulate Cardiac Membrane Protein Targeting
Hjalti Gudmundsson,Thomas J. Hund,Patrick J. Wright,Crystal F. Kline,Jedidiah S. Snyder,Lan Qian,Olha M. Koval,Shane R. Cunha,Manju George,Mark A. Rainey,Farshid Kashef,Wen Dun,Penelope A. Boyden,Mark E. Anderson,Hamid Band,Peter J. Mohler +15 more
TL;DR: The findings identify and characterize a new class of cardiac trafficking proteins, define the first group of proteins associated with the ankyrin-based targeting network, and identify potential new targets to modulate membrane excitability in disease.
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Mitochondrial calcium uniporter activity is dispensable for MDA-MB-231 breast carcinoma cell survival.
TL;DR: The conclusion that MDA-MB-231 breast cancer cells do not rely on MCU or MICU1 activity for survival in contrast to previous findings in cells derived from cervical, colon, and prostate cancers is supported and suggests that not all carcinomas will be sensitive to therapies targeting mitochondrial Ca2+ uptake mechanisms.
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Mitochondria-targeting particles
Amaraporn Wongrakpanich,Sean M. Geary,Mei Ling A. Joiner,Mark E. Anderson,Mark E. Anderson,Aliasger K. Salem +5 more
TL;DR: Recently reported strategies for delivering therapeutic molecules to mitochondria using various particle-based formulations are summarized.
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Oxidized Calmodulin Kinase II Regulates Conduction Following Myocardial Infarction: A Computational Analysis
Matthew D. Christensen,Wen Dun,Penelope A. Boyden,Mark E. Anderson,Peter J. Mohler,Thomas J. Hund +5 more
TL;DR: This work provides the first report of CaMKII oxidation state in a well-validated, large-animal model of heart disease and identifies a novel oxidation-dependent pathway for Ca MKII activation in the infarct BZ that may be an effective therapeutic target for improving conduction and reducing heterogeneity in theinfarcted heart.
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Calmodulin kinase II is required for angiotensin II-mediated vascular smooth muscle hypertrophy.
TL;DR: The studies identify a complete pathway for ANG II-triggered arterial VSM hypertrophy and identify new potential therapeutic targets for chronic human hypertension.