What is he best known for?
The fields of study he is best known for:
- Gene
- Internal medicine
- Cancer
Walter J. Koch focuses on Internal medicine, Endocrinology, Signal transduction, Beta adrenergic receptor kinase and Receptor.
His studies deal with areas such as In vivo and Cardiology as well as Internal medicine.
His research integrates issues of Calcium-binding protein and Genetically modified mouse in his study of Endocrinology.
His Signal transduction study is concerned with the larger field of Cell biology.
Walter J. Koch interconnects Cardiac myocyte, Agonist, G protein-coupled receptor kinase, G alpha subunit and Kinase in the investigation of issues within Beta adrenergic receptor kinase.
Walter J. Koch combines subjects such as Stimulation, Neuroscience and Transgene with his study of Receptor.
His most cited work include:
- Seven-transmembrane-spanning receptors and heart function (788 citations)
- Cardiac function in mice overexpressing the beta-adrenergic receptor kinase or a beta ARK inhibitor. (677 citations)
- A novel protective effect of erythropoietin in the infarcted heart (513 citations)
What are the main themes of his work throughout his whole career to date?
His primary areas of investigation include Internal medicine, Endocrinology, Heart failure, Receptor and Cell biology.
Much of his study explores Internal medicine relationship to Cardiology.
His Endocrinology study incorporates themes from Signal transduction, Transgene and Adrenergic receptor.
His research investigates the connection between Heart failure and topics such as Pharmacology that intersect with problems in Reperfusion injury.
The Receptor study which covers Kinase that intersects with Phosphorylation.
The Beta adrenergic receptor kinase study combines topics in areas such as Cardioprotection and G protein-coupled receptor kinase.
He most often published in these fields:
- Internal medicine (56.62%)
- Endocrinology (40.85%)
- Heart failure (27.13%)
What were the highlights of his more recent work (between 2015-2021)?
- Internal medicine (56.62%)
- Heart failure (27.13%)
- Cell biology (21.77%)
In recent papers he was focusing on the following fields of study:
His scientific interests lie mostly in Internal medicine, Heart failure, Cell biology, Receptor and Endocrinology.
In his study, which falls under the umbrella issue of Internal medicine, Sympathetic nervous system is strongly linked to Cardiology.
The study incorporates disciplines such as Fibrosis, Inflammation and Disease in addition to Heart failure.
Walter J. Koch has included themes like Kinase and Pharmacology in his Receptor study.
His Endocrinology research integrates issues from Apoptosis and Protein kinase B.
His Beta adrenergic receptor kinase research is multidisciplinary, incorporating elements of Downregulation and upregulation and G protein-coupled receptor kinase.
Between 2015 and 2021, his most popular works were:
- MCUR1 Is a Scaffold Factor for the MCU Complex Function and Promotes Mitochondrial Bioenergetics (117 citations)
- Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-Induced Endothelial Cell Activation (98 citations)
- Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis (86 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Internal medicine
- Cancer
His main research concerns Internal medicine, Beta adrenergic receptor kinase, Receptor, Heart failure and Endocrinology.
He works mostly in the field of Internal medicine, limiting it down to concerns involving Cardiology and, occasionally, Diastole.
The various areas that Walter J. Koch examines in his Beta adrenergic receptor kinase study include Protein kinase B and G protein-coupled receptor kinase.
His Receptor research is multidisciplinary, relying on both Immune system, Signal transduction, Pharmacology and Stimulation.
His Heart failure research includes themes of Inotrope, Moxonidine, Myocardial infarction and Sympathetic nervous system.
His biological study spans a wide range of topics, including Apoptosis and Ischemia.
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