Cell Signaling Technology

Protor-2 (D19A5) Rabbit Monoclonal Antibody

#12288 · $161

100
Citing papers
4.7k
Combined citations
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Research areas

Cardiac Fibrosis and Remodeling9Autophagy in Disease and Therapy8Redox biology and oxidative stress6Ubiquitin and proteasome pathways5Cardiomyopathy and Myosin Studies5Signaling Pathways in Disease5Birth, Development, and Health5Cell Adhesion Molecules Research4

Papers citing this product

1
Oxidant stress from nitric oxide synthase–3 uncoupling stimulates cardiac pathologic remodeling from chronic pressure load
Journal of Clinical Investigation·2005·445 cit.·DOI
2
Pivotal role of cardiomyocyte TGF-β signaling in the murine pathological response to sustained pressure overload
Journal of Clinical Investigation·2011·328 cit.·DOI
3
Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling
Journal of Clinical Investigation·2003·306 cit.·DOI
4
Activation of MAPK pathways links LMNA mutations to cardiomyopathy in Emery-Dreifuss muscular dystrophy
Journal of Clinical Investigation·2007·303 cit.·DOI
5
The role of the Grb2–p38 MAPK signaling pathway in cardiac hypertrophy and fibrosis
Journal of Clinical Investigation·2003·212 cit.·DOI
6
The Programming of Cardiac Hypertrophy in the Offspring by Maternal Obesity Is Associated with Hyperinsulinemia, AKT, ERK, and mTOR Activation
Endocrinology·2012·137 cit.·DOI
7
Reversal of Global Apoptosis and Regional Stress Kinase Activation by Cardiac Resynchronization
Circulation·2008·130 cit.·DOI
8
p38 MAPK Inhibition Improves Heart Function in Pressure-Loaded Right Ventricular Hypertrophy
American Journal of Respiratory Cell and Molecular Biology·2017·119 cit.·DOI
9
Mitogen-activated Protein Kinases p38 and ERK 1/2 Mediate the Wall Stress-induced Activation of GATA-4 Binding in Adult Heart
Journal of Biological Chemistry·2004·103 cit.·DOI
10
Paradoxical role of autophagy in the dysplastic and tumor-forming stages of hepatocarcinoma development in rats
Cell Death and Disease·2013·84 cit.·DOI