Thomas Force merges Kinase with MAPK/ERK pathway in his research. With his scientific publications, his incorporates both MAPK/ERK pathway and Kinase. His work on Cell biology is being expanded to include thematically relevant topics such as Protein kinase A. Thomas Force regularly links together related areas like Biochemistry in his Protein kinase A studies. Thomas Force incorporates Biochemistry and Molecular biology in his studies. While working in this field, Thomas Force studies both Molecular biology and Cell biology. Computer network is closely attributed to Terminal (telecommunication) in his research. His Terminal (telecommunication) study frequently links to other fields, such as Computer network. Thomas Force merges p38 mitogen-activated protein kinases with Mitogen-activated protein kinase in his study.
His Internal medicine study frequently draws parallels with other fields, such as Contraction (grammar). He regularly ties together related areas like Internal medicine in his Contraction (grammar) studies. His studies link Angiotensin II with Biochemistry. His research links Receptor with Angiotensin II. Many of his studies involve connections with topics such as Endothelin 1 and Receptor. Cell biology and Mitogen-activated protein kinase kinase are frequently intertwined in his study. Mitogen-activated protein kinase kinase and Cyclin-dependent kinase 9 are commonly linked in his work. In his works, he undertakes multidisciplinary study on Cyclin-dependent kinase 9 and Cyclin-dependent kinase 2. His research on Cyclin-dependent kinase 2 frequently links to adjacent areas such as Protein kinase A.
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Cardiotoxicity of the cancer therapeutic agent imatinib mesylate
Risto Kerkelä;Luanda Grazette;Rinat Yacobi;Cezar Iliescu.
Nature Medicine (2006)
Expert Consensus for Multimodality Imaging Evaluation of Adult Patients during and after Cancer Therapy: A Report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging.
Juan Carlos Plana;Maurizio Galderisi;Ana Barac;Michael S. Ewer.
Journal of The American Society of Echocardiography (2014)
Cardiotoxicity associated with tyrosine kinase inhibitor sunitinib
Tammy F Chu;Tammy F Chu;Maria A Rupnick;Maria A Rupnick;Risto Kerkela;Susan M Dallabrida.
The Lancet (2007)
Heart failure: preventing disease and death worldwide.
Piotr P. Ponikowski;Stefan D. Anker;Khalid F. AlHabib;Martin R. Cowie.
Esc Heart Failure (2014)
Expression cloning of a common receptor for parathyroid hormone and parathyroid hormone-related peptide from rat osteoblast-like cells: a single receptor stimulates intracellular accumulation of both cAMP and inositol trisphosphates and increases intracellular free calcium
A B Abou-Samra;H Jüppner;T Force;M W Freeman.
Proceedings of the National Academy of Sciences of the United States of America (1992)
Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition.
Thomas Force;Daniela S. Krause;Richard A. Van Etten.
Nature Reviews Cancer (2007)
Akt Activation Preserves Cardiac Function and Prevents Injury After Transient Cardiac Ischemia In Vivo
Takashi Matsui;Jingzang Tao;Federica del Monte;Kyung-Han Lee.
Protein kinase cascades in the regulation of cardiac hypertrophy
Gerald W. Dorn;Thomas Force.
Journal of Clinical Investigation (2005)
Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.
Beth A. Rose;Thomas Force;Yibin Wang.
Physiological Reviews (2010)
Glycogen Synthase Kinase-3β Is a Negative Regulator of Cardiomyocyte Hypertrophy
Syed Haq;Gabriel Choukroun;Zhao Bin Kang;Hardeep Ranu.
Journal of Cell Biology (2000)
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