Beverly A. Rothermel spends much of her time researching Internal medicine, Endocrinology, Calcineurin, Myocyte and Cell biology. In Endocrinology, she works on issues like FOXO1, which are connected to FOXO3. Her Calcineurin research includes themes of Phosphatase, Gene expression, In vivo and Skeletal muscle.
The concepts of her Myocyte study are interwoven with issues in Myocardial infarction, Biochemistry, Heart failure and Regeneration. The Cell biology study which covers Autophagy that intersects with Protein aggregation. Her studies deal with areas such as Programmed cell death and Pathogenesis as well as Pressure overload.
Beverly A. Rothermel mainly focuses on Cell biology, Internal medicine, Endocrinology, Calcineurin and Autophagy. Her studies link Programmed cell death with Cell biology. Muscle hypertrophy, Heart failure, Myocyte and Pressure overload are the subjects of her Internal medicine studies.
In her study, FOXO3 is strongly linked to FOXO1, which falls under the umbrella field of Endocrinology. Her Calcineurin research also works with subjects such as
Her primary areas of study are Cell biology, Calcineurin, Mitochondrion, Internal medicine and Heart failure. Her Cell biology study often links to related topics such as Knockout mouse. Her study in the field of NFAT is also linked to topics like Dynamics.
Her Mitochondrion study combines topics from a wide range of disciplines, such as Unfolded protein response, Phosphatase, Programmed cell death and Homeostasis. Her Internal medicine research is multidisciplinary, incorporating perspectives in Endocrinology and Cardiology. Her Heart failure research incorporates themes from Autophagy, Mitophagy and Bioinformatics.
Her primary areas of investigation include Cell biology, Autophagy, Bioinformatics, Heart failure and Mitochondrion. Her research on Autophagy also deals with topics like
Beverly A. Rothermel has included themes like Protein kinase A, Phosphorylation, Unfolded protein response, Endoplasmic reticulum and Programmed cell death in her Mitochondrion study. Her research integrates issues of Endocrinology and Internal medicine in her study of Cell growth. Her NFAT and Calcineurin study in the realm of Internal medicine interacts with subjects such as TRPC.
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Cardiac autophagy is a maladaptive response to hemodynamic stress
Hongxin Zhu;Paul Tannous;Janet L. Johnstone;Yongli Kong.
Journal of Clinical Investigation (2007)
Regulation of neonatal and adult mammalian heart regeneration by the miR-15 family
Enzo R. Porrello;Ahmed I. Mahmoud;Emma Simpson;Brett A. Johnson.
Proceedings of the National Academy of Sciences of the United States of America (2013)
The oxygen-rich postnatal environment induces cardiomyocyte cell-cycle arrest through DNA damage response.
Bao N. Puente;Wataru Kimura;Shalini A. Muralidhar;Jesung Moon.
A protein encoded within the Down syndrome critical region is enriched in striated muscles and inhibits calcineurin signaling
Beverly A Rothermel;Rick B. Vega;John Yang;Hai Wu.
Journal of Biological Chemistry (2000)
Increased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress
Roberto Bravo;Jose Miguel Vicencio;Jose Miguel Vicencio;Valentina Parra;Rodrigo Troncoso.
Journal of Cell Science (2011)
Activation of MEF2 by muscle activity is mediated through a calcineurin-dependent pathway.
Hai Wu;Beverly A Rothermel;Shane Kanatous;Paul Rosenberg.
The EMBO Journal (2001)
Independent Signals Control Expression of the Calcineurin Inhibitory Proteins MCIP1 and MCIP2 in Striated Muscles
J. Yang;B. Rothermel;R. B. Vega;N. Frey.
Circulation Research (2000)
Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo.
Beverly A Rothermel;Timothy A. McKinsey;Rick B. Vega;Rebekka L. Nicol.
Proceedings of the National Academy of Sciences of the United States of America (2001)
Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy
Dian J. Cao;Zhao V. Wang;Pavan K. Battiprolu;Nan Jiang.
Proceedings of the National Academy of Sciences of the United States of America (2011)
Suppression of Class I and II Histone Deacetylases Blunts Pressure-Overload Cardiac Hypertrophy
Yongli Kong;Paul Tannous;Guangrong Lu;Kambeez Berenji.
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