What is he best known for?
The fields of study he is best known for:
- Gene
- DNA
- Internal medicine
The scientist’s investigation covers issues in Myocyte, Calcineurin, Cell biology, Skeletal muscle and Gene expression.
Endocrinology and Internal medicine are the subject areas of his Myocyte study.
His Calcineurin study typically links adjacent topics like Mef2.
His Cell biology research incorporates themes from Molecular biology, E2F and NFAT.
His Skeletal muscle study integrates concerns from other disciplines, such as Calcium, Muscle contraction and Mitochondrial biogenesis.
His research investigates the connection between Gene expression and topics such as Cyclosporin a that intersect with problems in Cardiac muscle, Muscle hypertrophy and ITGA7.
His most cited work include:
- A calcineurin-dependent transcriptional pathway controls skeletal muscle fiber type (889 citations)
- A calcineurin-dependent transcriptional pathway controls skeletal muscle fiber type (889 citations)
- Regulation of mitochondrial biogenesis in skeletal muscle by CaMK. (567 citations)
What are the main themes of his work throughout his whole career to date?
His primary scientific interests are in Cell biology, Internal medicine, Skeletal muscle, Endocrinology and Myocyte.
His Cell biology research includes themes of Molecular biology, Regulation of gene expression and Transcription factor, NFAT.
His research ties Cardiology and Internal medicine together.
His Skeletal muscle study combines topics in areas such as Biochemistry, Myoglobin, Muscle contraction, Muscle hypertrophy and Mitochondrial biogenesis.
His Myocyte study which covers Calcineurin that intersects with Gene expression.
R. Sanders Williams combines subjects such as Cyclosporin a and In vivo with his study of Gene expression.
He most often published in these fields:
- Cell biology (43.56%)
- Internal medicine (44.55%)
- Skeletal muscle (34.65%)
What were the highlights of his more recent work (between 2003-2015)?
- Cell biology (43.56%)
- Skeletal muscle (34.65%)
- Myocyte (23.76%)
In recent papers he was focusing on the following fields of study:
His primary areas of investigation include Cell biology, Skeletal muscle, Myocyte, Internal medicine and Endocrinology.
His work carried out in the field of Cell biology brings together such families of science as Regulation of gene expression, Biochemistry and Transcription factor.
His work deals with themes such as Angiogenesis, Endurance training, Transient receptor potential channel, Muscle contraction and Muscle hypertrophy, which intersect with Skeletal muscle.
R. Sanders Williams has included themes like Reporter gene, Mef2 and Mitochondrial biogenesis in his Internal medicine study.
His work in the fields of Denervation overlaps with other areas such as CAMK and GLUT4.
His studies deal with areas such as Gene expression and Cell type as well as NFAT.
Between 2003 and 2015, his most popular works were:
- Exercise Stimulates Pgc-1α Transcription in Skeletal Muscle through Activation of the p38 MAPK Pathway (522 citations)
- STIM1 signalling controls store-operated calcium entry required for development and contractile function in skeletal muscle (281 citations)
- Renaming the DSCR1/Adapt78 gene family as RCAN: regulators of calcineurin (136 citations)
In his most recent research, the most cited papers focused on:
- Gene
- DNA
- Internal medicine
His main research concerns Cell biology, Skeletal muscle, Internal medicine, Endocrinology and Muscle contraction.
R. Sanders Williams integrates many fields in his works, including Cell biology and Humanities.
His Skeletal muscle research is multidisciplinary, incorporating perspectives in Myocyte and Tissue engineering.
The concepts of his Myocyte study are interwoven with issues in Laminin, Fibronectin, Extracellular matrix and Biochemistry.
His research in Internal medicine intersects with topics in Gene expression, Cell type and Mitochondrial biogenesis.
His studies in Endocrinology integrate themes in fields like Transcription factor, NFAT, Calcineurin and Transient receptor potential channel.
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