Raisa Klevitsky

PKA-dependent phosphorylation of cardiac myosin binding protein C in transgenic mice (2001)

Yang, Qinglin, Hewett, Timothy E., Klevitsky, Raisa, Sanbe, Atsushi, Wang, Xuejun, Robbins, Jeffrey

Objective: To investigate the physiological role of cAMP-dependent protein kinase A (PKA)-mediated, cardiac myosin binding protein C (MyBP-C) phosphorylation. Methods: A cardiac MyBP-C cDNA lacking...

Hypertrophic defect unmasked by calcineurin expression in asymptomatic tropomodulin overexpressing transgenic mice (2000)

Sussman, Mark A., Welch, Sara, Walker, Angela, Klevitsky, Raisa, Hewett, Timothy E., Witt, Sandra A., ...

Objective: Dilation and hypertrophy often occur concurrently in cardiomyopathy, yet the interaction between these two functionally distinct conditions remains unknown. Methods: Combinatorial effects...

The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice

Bueno, Orlando F., De Windt, Leon J., Tymitz, Kevin M., Witt, Sandra A., Kimball, Thomas R., Klevitsky, Raisa, ...

Members of the mitogen-activated protein kinase (MAPK) cascade such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 are implicated as important regulators of...

Altered focal adhesion regulation correlates with cardiomyopathy in mice expressing constitutively active rac1

Sussman, Mark A., Welch, Sara, Walker, Angela, Klevitsky, Raisa, Hewett, Timothy E., Price, Robert L., ...

The ras family of small GTP-binding proteins exerts powerful effects upon cell structure and function. One member of this family, rac, induces actin cytoskeletal reorganization in nonmuscle cells and...

Proinflammatory consequences of transgenic Fas ligand expression in the heart

Nelson, David P., Setser, Elizabeth, Hall, D. Greg, Schwartz, Steven M., Hewitt, Timothy, Klevitsky, Raisa, ...

Expression of Fas ligand (FasL) renders certain tissues immune privileged, but its expression in other tissues can result in severe neutrophil infiltration and tissue destruction. The consequences of...

Reversal of amyloid-induced heart disease in desmin-related cardiomyopathy

Sanbe, Atsushi, Osinska, Hanna, Villa, Chet, Gulick, James, Klevitsky, Raisa, Glabe, Charles G., ...

Amyloid oligomers, similar to the toxic entities found in Alzheimer's disease patients and in other amyloid-based diseases, are present in cardiomyocytes derived from human heart-failure patients and...

Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling

Braz, Julian C., Bueno, Orlando F., Liang, Qiangrong, Wilkins, Benjamin J., Dai, Yan-Shan, Parsons, Stephanie, ...

The MAPKs are important transducers of growth and stress stimuli in virtually all eukaryotic cell types. In the mammalian heart, MAPK signaling pathways have been hypothesized to regulate myocyte...

Cardiac Myosin Binding Protein-C Phosphorylation and Cardiac Function

Sadayappan, Sakthivel, Gulick, James, Osinska, Hanna, Martin, Lisa A., Hahn, Harvey S., Dorn, Gerald W., ...

The role of cardiac myosin binding protein-C (cMyBP-C) phosphorylation in cardiac physiology or pathophysiology is unclear. To investigate the status of cMyBP-C phosphorylation in vivo, we determined...

Charged residue alterations in the inner-core domain and carboxy-terminus of α-tropomyosin differentially affect mouse cardiac muscle contractility

Gaffin, Robert D, Tong, Carl W, Zawieja, David C, Hewett, Timothy E, Klevitsky, Raisa, Robbins, Jeffrey, ...

Two important charge differences between the α- and β-tropomyosin (TM) isoforms are the exchange of a serine residue in the inner-core region at position 229, and a histidine residue at the...

Charged residue changes in the carboxy-terminus of α-tropomyosin alter mouse cardiac muscle contractility

Gaffin, Robert D, Gokulan, Kuppan, Sacchettini, James C, Hewett, Timothy, Klevitsky, Raisa, Robbins, Jeffrey, ...

Striated muscle tropomyosin (TM) is an essential thin filament protein that is sterically and allosterically involved in calcium-mediated cardiac contraction. We have previously shown that...

Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling

Braz, Julian C., Bueno, Orlando F., Liang, Qiangrong, Wilkins, Benjamin J., Dai, Yan-Shan, Parsons, Stephanie, ...

The MAPKs are important transducers of growth and stress stimuli in virtually all eukaryotic cell types. In the mammalian heart, MAPK signaling pathways have been hypothesized to regulate myocyte...

The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice

Bueno, Orlando F., De Windt, Leon J., Tymitz, Kevin M., Witt, Sandra A., Kimball, Thomas R., Klevitsky, Raisa, ...

Members of the mitogen-activated protein kinase (MAPK) cascade such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 are implicated as important regulators of...

Altered focal adhesion regulation correlates with cardiomyopathy in mice expressing constitutively active rac1

Sussman, Mark A., Welch, Sara, Walker, Angela, Klevitsky, Raisa, Hewett, Timothy E., Price, Robert L., ...

The ras family of small GTP-binding proteins exerts powerful effects upon cell structure and function. One member of this family, rac, induces actin cytoskeletal reorganization in nonmuscle cells and...

Proinflammatory consequences of transgenic Fas ligand expression in the heart

Nelson, David P., Setser, Elizabeth, Hall, D. Greg, Schwartz, Steven M., Hewitt, Timothy, Klevitsky, Raisa, ...

Expression of Fas ligand (FasL) renders certain tissues immune privileged, but its expression in other tissues can result in severe neutrophil infiltration and tissue destruction. The consequences of...

Reversal of amyloid-induced heart disease in desmin-related cardiomyopathy

Sanbe, Atsushi, Osinska, Hanna, Villa, Chet, Gulick, James, Klevitsky, Raisa, Glabe, Charles G., ...

Amyloid oligomers, similar to the toxic entities found in Alzheimer's disease patients and in other amyloid-based diseases, are present in cardiomyocytes derived from human heart-failure patients and...

Charged residue changes in the carboxy-terminus of α-tropomyosin alter mouse cardiac muscle contractility

Gaffin, Robert D, Gokulan, Kuppan, Sacchettini, James C, Hewett, Timothy, Klevitsky, Raisa, Robbins, Jeffrey, ...

Striated muscle tropomyosin (TM) is an essential thin filament protein that is sterically and allosterically involved in calcium-mediated cardiac contraction. We have previously shown that...

Charged residue alterations in the inner-core domain and carboxy-terminus of α-tropomyosin differentially affect mouse cardiac muscle contractility

Gaffin, Robert D, Tong, Carl W, Zawieja, David C, Hewett, Timothy E, Klevitsky, Raisa, Robbins, Jeffrey, ...

Two important charge differences between the α- and β-tropomyosin (TM) isoforms are the exchange of a serine residue in the inner-core region at position 229, and a histidine residue at the...

Cardiac myosin binding protein c phosphorylation is cardioprotective

Sadayappan, Sakthivel, Osinska, Hanna, Klevitsky, Raisa, Lorenz, John N., Sargent, Michelle, Molkentin, Jeffrey D., ...

Cardiac myosin binding protein C (cMyBP-C) has three phosphorylatable serines at its N terminus (Ser-273, Ser-282, and Ser-302), and the residues' phosphorylation states may alter thick filament...

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure

Nakayama, Hiroyuki, Chen, Xiongwen, Baines, Christopher P., Klevitsky, Raisa, Zhang, Xiaoying, Zhang, Hongyu, ...

Loss of cardiac myocytes in heart failure is thought to occur largely through an apoptotic process. Here we show that heart failure can also be precipitated through myocyte necrosis associated with...

Cardiomyocyte GATA4 functions as a stress-responsive regulator of angiogenesis in the murine heart

Heineke, Joerg, Auger-Messier, Mannix, Xu, Jian, Oka, Toru, Sargent, Michelle A., York, Allen, ...

The transcription factor GATA4 is a critical regulator of cardiac gene expression, modulating cardiomyocyte differentiation and adaptive responses of the adult heart. We report what we believe to be...