John W. Adams - Concepedia

Author

John W. Adams

University of California San Diego

Also Known As

J W ADAMS, JOHN W. ADAMS, John Adams, John W Adams, John W. Adams

Publications

1.7K

Citations

H-Index

Concepts

All Affiliations

University of California San Diego Arena Pharmaceuticals (United States)University of Cincinnati Beacon Clinical Research Virginia Commonwealth University Medical Center

About

John W. Adams is an author at University of California San Diego specializing in medicine, cell signaling, and molecular physiology.

Top Concepts

#	Concept	H-Index	Publications	Citations
1	Medicine	10	10	559
2	Cellular Physiology	8	8	468
3	Cell Biology	7	7	440
4	Natural Sciences	1	1	64
5	Biochemistry	1	1	64

John W. Adams

Publications

1.6K

Citations

H-Index

Page 1

	Year	Citations
Enhanced Gαq signaling: A common pathway mediates cardiac hypertrophy and apoptotic heart failure John W. Adams, Yoshihito Sakata, Michael Davis, Proceedings of the National Academy of Sciences	1998	533
G Alpha-q/11 Protein Plays a Key Role in Insulin-Induced Glucose Transport in 3T3-L1 Adipocytes Takeshi Imamura, Péter Vollenweider, Katsuya Egawa, Molecular and Cellular Biology	1999	182
Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes John W. Adams, Darren S. Migita, Maggie Yu, Journal of Biological Chemistry Cardiac MuscleCell GrowthCellular PhysiologyProstaglandin F2 AlphaFibroblast Growth Factor	1996	107
Cardiomyocyte Apoptosis Induced by Gαq Signaling Is Mediated by Permeability Transition Pore Formation and Activation of the Mitochondrial Death Pathway John W. Adams, Amy L. Pagel, Christopher K. Means, Circulation Research	2000	105
Lysophosphatidic acid induces hypertrophy of neonatal cardiac myocytes via activation of Gi and Rho Randa Hilal-Dandan, Christopher K. Means, Åsa B. Gustafsson, Journal of Molecular and Cellular Cardiology Cardiac MuscleCardiomyopathyMolecular PhysiologyCell SignalingPhysiology	2004	71
Akt-mediated Cardiomyocyte Survival Pathways Are Compromised by Gαq-induced Phosphoinositide 4,5-Bisphosphate Depletion Amy L. Howes, Jane F. Arthur, Tong Zhang, Journal of Biological Chemistry Cardiac MuscleHeart FailureApoptosisCell DeathCellular Physiology	2003	68
Ca2+ Dysregulation Induces Mitochondrial Depolarization and Apoptosis Shigeki Miyamoto, Amy L. Howes, John W. Adams, Journal of Biological Chemistry Cell PhysiologySr CaSignal TransductionMolecular PhysiologyMitochondrial Function	2005	64
Tyrosine Kinase and c-Jun NH<sub>2</sub>-Terminal Kinase Mediate Hypertrophic Responses to Prostaglandin F<sub>2α</sub>in Cultured Neonatal Rat Ventricular Myocytes John W. Adams, Valerie P. Sah, Scott A. Henderson, Circulation Research	1998	61
Angiotensin (1–7) does not interact directly with MAS1, but can potently antagonize signaling from the AT1 receptor Ibragim Gaidarov, John W. Adams, John Frazer, Cellular Signalling InflammationMolecular PharmacologyAt1 ReceptorSignal TransductionMolecular Physiology	2018	56
Myocardial expression, signaling, and function of GPR22: a protective role for an orphan G protein-coupled receptor John W. Adams, Jianming Wang, James R. Davis, American Journal of Physiology-Heart and Circulatory Physiology Cardiac MuscleCellular PhysiologyMolecular PharmacologyOrphan Gpr22Gpr22 Mrna	2008	52

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