Deletion of Ptpn11 (Shp2) in Cardiomyocytes Causes Dilated Cardiomyopathy via Effects on the Extracellular Signal–Regulated Kinase/Mitogen-Activated Protein Kinase and RhoA Signaling Pathways | Zendy

Maria I. Kontaridis | Zendy; Wentian Yang | Zendy; Kendra K. Bence | Zendy; Darragh Cullen | Zendy; Bo Wang | Zendy; Natalya D. Bodyak | Zendy; Qingen Ke | Zendy; Aleksander Hinek | Zendy; Peter M. Kang | Zendy; Ronglih Liao | Zendy; Benjamin G. Neel | Zendy

Open Access

Deletion of Ptpn11 (Shp2) in Cardiomyocytes Causes Dilated Cardiomyopathy via Effects on the Extracellular Signal–Regulated Kinase/Mitogen-Activated Protein Kinase and RhoA Signaling Pathways

Author(s) -

Maria I. Kontaridis,

Wentian Yang,

Kendra K. Bence,

Darragh Cullen,

Bo Wang,

Natalya D. Bodyak,

Qingen Ke,

Aleksander Hinek,

Peter M. Kang,

Ronglih Liao,

Benjamin G. Neel

Publication year - 2008

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.107.728865

Subject(s) - rhoa , mapk/erk pathway , signal transduction , protein tyrosine phosphatase , medicine , microbiology and biotechnology , pressure overload , kinase , protein kinase a , cancer research , biology , muscle hypertrophy , cardiac hypertrophy

Heart failure is the leading cause of death in the United States. By delineating the pathways that regulate cardiomyocyte function, we can better understand the pathogenesis of cardiac disease. Many cardiomyocyte signaling pathways activate protein tyrosine kinases. However, the role of specific protein tyrosine phosphatases (PTPs) in these pathways is unknown.

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