Elizabeth D. Luczak

发表

Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy

Mark E. Anderson, A. Heck, R. Weiss, 2020, Nature Communications.

Oxidation of CaMKII determines the cardiotoxic effects of aldosterone

Mark E. Anderson, S. Heymans, R. Weiss, 2011, Nature Medicine.

Soy diet worsens heart disease in mice.

L. Leinwand, B. Stauffer, J. Konhilas, 2005 .

Cyclin D2 is a critical mediator of exercise-induced cardiac hypertrophy

L. Leinwand, J. Konhilas, Elizabeth D. Luczak, 2017, Experimental biology and medicine.

The Multifunctional Ca2+/Calmodulin-Dependent Kinase IIδ (CaMKIIδ) Regulates Arteriogenesis in a Mouse Model of Flow-Mediated Remodeling

Mark E. Anderson, R. Weiss, J. Backs, 2013, PloS one.

Oxidative activation of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) regulates vascular smooth muscle migration and apoptosis.

Mark E. Anderson, Elizabeth D. Luczak, Omar A Jaffer, 2014, Vascular pharmacology.

CaMKII determines mitochondrial stress responses in heart

Mark E. Anderson, D. Hall, T. Scholz, 2012, Nature.

CaMKII effects on inotropic but not lusitropic force frequency responses require phospholamban.

Mark E. Anderson, X. Wehrens, H. Granzier, 2012, Journal of molecular and cellular cardiology.

CaMKII exacerbates heart failure progression by activating class I HDACs.

Xue Yang, Hong Jiang, M. Ross, 2020, Journal of molecular and cellular cardiology.

CaMKII Is Essential for the Proasthmatic Effects of Oxidation

Mark E. Anderson, P. Howarth, D. Meyerholz, 2013, Science Translational Medicine.

Catecholamine-Independent Heart Rate Increases Require Ca2+/Calmodulin-Dependent Protein Kinase II

Mark E. Anderson, D. Hall, Long-Sheng Song, 2011, Circulation. Arrhythmia and electrophysiology.

Regulation of Cardiac ATP-sensitive Potassium Channel Surface Expression by Calcium/Calmodulin-dependent Protein Kinase II*

Mark E. Anderson, Zhiyong Zhu, L. Zingman, 2012, The Journal of Biological Chemistry.

Diet and sex modify exercise and cardiac adaptation in the mouse.

B. LaFleur, L. Leinwand, T. McKinsey, 2015, American journal of physiology. Heart and circulatory physiology.

Oxidized CaMKII promotes asthma through the activation of mast cells.

Mark E. Anderson, W. Mitzner, P. Gao, 2017, JCI insight.

MyD88 mediated inflammatory signaling leads to CaMKII oxidation, cardiac hypertrophy and death after myocardial infarction.

Mark E. Anderson, R. Weiss, W. Kutschke, 2012, Journal of molecular and cellular cardiology.

Joiner et al. reply

Mark E. Anderson, D. Hall, T. Scholz, 2014, Nature.

Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart

Mark E. Anderson, F. Zhan, Liping Yu, 2015, Proceedings of the National Academy of Sciences.

MICAL1 constrains cardiac stress responses and protects against disease by oxidizing CaMKII.

Vassilios J. Bezzerides, A. Kolodkin, W. Pu, 2020, Journal of Clinical Investigation.

CaMKII oxidative activation and the pathogenesis of cardiac disease.

Elizabeth D. Luczak, M. Anderson, 2014, Journal of molecular and cellular cardiology.

Genome-wide CRISPR screen reveals genetic modifiers of Ca2+-mediated cell death

Elizabeth D. Luczak, Oscar E. Reyes Gaido, M. Anderson, 2023, bioRxiv.

Correction: Corrigendum: The mitochondrial uniporter controls fight or flight heart rate increases

Yuejin Wu, Long-Sheng Song, D. Hall, 2015, Nature Communications.

Oxidized Ca2+/Calmodulin-Dependent Protein Kinase II Triggers Atrial Fibrillation

R. Weiss, X. Wehrens, Long-Sheng Song, 2013, Circulation.

Oxidized-CaMKII and O-GlcNAcylation cause increased atrial fibrillation in diabetic mice by distinct mechanisms.

R. Cole, G. Hart, T. Boronina, 2020, The Journal of clinical investigation.

O-GlcNAcylation, oxidation and CaMKII contribute to atrial fibrillation in type 1 and type 2 diabetes by distinct mechanisms

R. Cole, G. Hart, T. Boronina, 2020, bioRxiv.

O-GlcNAcylation and oxidation contribute to atrial fibrillation in diabetes by activating CaMKII

G. Hart, R. Ahima, X. Wehrens, 2020 .

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

Niels Voigt, Igor Efimov, Masahiro Ogawa, 2011, The Journal of clinical investigation.

Sex-based cardiac physiology.

L. Leinwand, Elizabeth D. Luczak, 2009, Annual review of physiology.

Excessive O-GlcNAcylation Causes Heart Failure and Sudden Death

G. Hart, L. Florea, An-Chi Wei, 2021, Circulation.

Diabetes increases mortality after myocardial infarction by oxidizing CaMKII.

I. Efimov, R. Weiss, L. Maier, 2013, The Journal of clinical investigation.

Catecholamine-Independent Heart Rate Increases Require CaMKII

D. Hall, Long-Sheng Song, P. Mohler, 2011 .

Novel Biosensor Identifies Ruxolitinib as a Potent and Cardioprotective CaMKII Inhibitor

Jun O. Liu, Elizabeth D. Luczak, Jonathan M. Granger, 2022, bioRxiv.

Remodeling the cardiac transcriptional landscape with diet.

L. Leinwand, Tom H. Cheung, B. Stauffer, 2011, Physiological genomics.

Excessive O - GlcNAcylation causes heart failure and sudden death

G. Hart, L. Florea, An-Chi Wei, 2020, bioRxiv.

The mitochondrial uniporter controls fight or flight heart rate increases

D. Hall, X. Wehrens, Long-Sheng Song, 2015, Nature Communications.

Estrogenic compounds are not always cardioprotective and can be lethal in males with genetic heart disease.

L. Leinwand, P. Watson, B. Stauffer, 2012, Endocrinology.

Soy diet worsens heart disease in mice.

L. Leinwand, B. Stauffer, J. Konhilas, 2005, The Journal of clinical investigation.

Mitochondrial CaMKII causes metabolic reprogramming, energetic insufficiency, and dilated cardiomyopathy

A. Heck, R. Weiss, An-Chi Wei, 2020, bioRxiv.

Oxidative stress–induced autonomous activation of the calcium/calmodulin-dependent kinase II involves disulfide formation in the regulatory domain

R. Levine, Geumsoo Kim, Yi He, 2022, The Journal of biological chemistry.

wheel running in the mouse Cardiac and skeletal muscle adaptations to voluntary

Rick B. Vega, B. LaFleur, B. Harrison, 2015 .

An improved reporter identifies ruxolitinib as a potent and cardioprotective CaMKII inhibitor

Vassilios J. Bezzerides, R. Huganir, X. Wehrens, 2023, Science Translational Medicine.

CaV1.2 β-subunit coordinates CaMKII-triggered cardiomyocyte death and afterdepolarizations

R. Colbran, P. Mohler, T. Hund, 2010, Proceedings of the National Academy of Sciences.

CaMKII as a Therapeutic Target in Cardiovascular Disease

Klitos Konstantinidis, P. Umapathi, Elizabeth D. Luczak, 2022, Annual review of pharmacology and toxicology.

Dysregulation of cardiac CaMKII pathway is increased in aging and chronic inflammation

J. Walston, J. Zhuo, R. Marx, 2021, The FASEB Journal.

Sex-based cardiac physiology.

L. Leinwand, Elizabeth D. Luczak, 2009, Annual Review of Physiology.

Diabetes increases mortality after myocardial infarction by oxidizing CaMKII.

I. Efimov, R. Weiss, L. Maier, 2013, The Journal of clinical investigation.

Diabetes Increases Mortality after Myocardial Infarction by Oxidizing Camkii Recommended Citation Diabetes Increases Mortality after Myocardial Infarction by Oxidizing Camkii Diabetes Increases Oxidant Stress and Doubles the Risk of Dying after Myocardial Infarction, but the Mecha- Nisms Underlying

T. Hund, W. Kutschke, P. Swaminathan, 2022 .

dietthe cardiac transcriptional landscape with

B. LaFleur, L. Leinwand, Tom H. Cheung, 2015 .

CaV1.2 β-subunit coordinates CaMKII-triggered cardiomyocyte death and afterdepolarizations

R. Colbran, P. Mohler, T. Hund, 2010, Proceedings of the National Academy of Sciences.

Joiner et al. reply

D. Hall, T. Scholz, Long-Sheng Song, 2014, Nature.