Craig A. Harrison mostly deals with Internal medicine, Endocrinology, Cell biology, Signal transduction and Myostatin. The study incorporates disciplines such as Endothelial stem cell and Bone morphogenetic protein 15 in addition to Internal medicine. He studies Endocrinology, focusing on Lipopolysaccharide in particular.
The Signal transduction study which covers Growth differentiation factor that intersects with Protein structure and Signal peptide. His research in Myostatin intersects with topics in Protein kinase B, PI3K/AKT/mTOR pathway and Bone morphogenetic protein 7. His Activin type 2 receptors study incorporates themes from Activin receptor, Cripto, ACVR1 and Follistatin.
His main research concerns Internal medicine, Endocrinology, Cell biology, Receptor and Signal transduction. His work deals with themes such as Biological activity and Bone morphogenetic protein, which intersect with Internal medicine. The Activin type 2 receptors, Sertoli cell and TGF beta signaling pathway research Craig A. Harrison does as part of his general Endocrinology study is frequently linked to other disciplines of science, such as Growth differentiation factor-9, therefore creating a link between diverse domains of science.
His Cell biology study integrates concerns from other disciplines, such as Growth differentiation factor and Myostatin. His biological study deals with issues like Binding site, which deal with fields such as Mutant, Peptide sequence and Inhibin binding. His Signal transduction study combines topics in areas such as Cripto and Structure–activity relationship.
His scientific interests lie mostly in Endocrinology, Internal medicine, Cancer research, Receptor and Bone morphogenetic protein 15. His biological study spans a wide range of topics, including Mutation and Mutagenesis. He combines subjects such as Andrology and Binding site with his study of Internal medicine.
He has researched Receptor in several fields, including Signal transduction, Cell biology and Bone morphogenetic protein. He is studying Transforming growth factor, which is a component of Cell biology. In his work, Cachexia, Muscle hypertrophy and Myostatin is strongly intertwined with Muscle atrophy, which is a subfield of Follistatin.
Craig A. Harrison spends much of his time researching Internal medicine, Endocrinology, Growth differentiation factor-9, Bone morphogenetic protein 15 and Atrophy. His study of Growth differentiation factor-9 brings together topics like Granulosa cell, Granulosa Lutein Cell, INHBB, Ovarian follicle and Polycystic ovary. His Andrology research extends to Bone morphogenetic protein 15, which is thematically connected.
Craig A. Harrison interconnects Muscle hypertrophy, Myostatin, Skeletal muscle, Cachexia and Wasting in the investigation of issues within Atrophy. His Wasting research integrates issues from Systemic administration and Protein degradation.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Targeting TGF-β Mediated SMAD Signaling for the Prevention of Fibrosis
Kelly L. Walton;Katharine E. Johnson;Craig A. Harrison.
Frontiers in Pharmacology (2017)
Antagonists of activin signaling: mechanisms and potential biological applications
Craig A. Harrison;Craig A. Harrison;Peter C. Gray;Wylie W. Vale;David M. Robertson.
Trends in Endocrinology and Metabolism (2005)
Follistatin-mediated skeletal muscle hypertrophy is regulated by Smad3 and mTOR independently of myostatin
Catherine E. Winbanks;Kate L. Weeks;Rachel E. Thomson;Patricio V. Sepulveda;Patricio V. Sepulveda.
Journal of Cell Biology (2012)
Cripto forms a complex with activin and type II activin receptors and can block activin signaling.
Peter C. Gray;Craig A. Harrison;Wylie Vale.
Proceedings of the National Academy of Sciences of the United States of America (2003)
Elevated expression of activins promotes muscle wasting and cachexia
Justin L. Chen;Justin L. Chen;Kelly L. Walton;Catherine E. Winbanks;Kate T. Murphy.
The FASEB Journal (2014)
The bone morphogenetic protein axis is a positive regulator of skeletal muscle mass
Catherine E Winbanks;Justin Chen;Justin Chen;Justin Chen;Hongwei Qian;Yingying Liu.
Journal of Cell Biology (2013)
Oxidation Regulates the Inflammatory Properties of the Murine S100 Protein S100A8
Craig A. Harrison;Mark J. Raftery;John Walsh;Paul Alewood.
Journal of Biological Chemistry (1999)
Inhibin and premature ovarian failure
AL Chand;CA Harrison;Andrew Shelling.
Human Reproduction Update (2010)
An activin mutant with disrupted ALK4 binding blocks signaling via type II receptors
Craig A. Harrison;Peter C. Gray;Wolfgang H. Fischer;Cindy Donaldson.
Journal of Biological Chemistry (2004)
Prodomains regulate the synthesis, extracellular localisation and activity of TGF-β superfamily ligands
Craig A. Harrison;Sara L. Al-Musawi;Kelly L. Walton.
Growth Factors Journal (2011)
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