Bethel Stannard - Concepedia

Author

Bethel Stannard

Also Known As

B S Stannard, B Stannard, B. S. Stannard, B. Stannard, B.S. Stannard, BETHEL S. STANNARD, Bethel S. Stannard, Bethel Stannard

Publications

4.9K

Citations

H-Index

Concepts

All Affiliations

National Institutes of Health National Institute of Diabetes and Digestive and Kidney Diseases National Institute of Arthritis and Musculoskeletal and Skin Diseases

About

Bethel Stannard is an author at National Institutes of Health specializing in medicine, endocrinology, and cell biology.

Top Concepts

#	Concept	H-Index	Publications	Citations
1	Medicine	23	28	3.7K
2	Health Sciences	8	8	2.2K
3	Natural Sciences	5	5	233
4	Engineering	3	3	260
5	Public Health	1	1	31

Bethel Stannard

Publications

4.6K

Citations

H-Index

Page 1

	Year	Citations
Normal growth and development in the absence of hepatic insulin-like growth factor I Shoshana Yakar, Jun‐Li Liu, Bethel Stannard, Proceedings of the National Academy of Sciences Igf1 MrnaHuman GrowthImmunologyPathologyInsulin Signaling	1999	1.4K
Role of tyrosine kinase activity in signal transduction by the insulin-like growth factor-I (IGF-I) receptor. Characterization of kinase-deficient IGF-I receptors and the action of an IGF-I-mimetic antibody (alpha IR-3). H. Kato, Teresa N. Faria, Bethel Stannard, Journal of Biological Chemistry Kinase-deficient Igf-i ReceptorsHuman GrowthImmunologyIgf-i ReceptorInsulin Signaling	1993	245
Inhibition of growth hormone action improves insulin sensitivity in liver IGF-1–deficient mice Shoshana Yakar, Jennifer Setser, Hong Zhao, Journal of Clinical Investigation Lid MiceInsulin SignalingObesityMetabolic SyndromeBody Composition	2004	231
Inhibition of growth hormone action improves insulin sensitivity in liver IGF-1–deficient mice Shoshana Yakar, Jennifer Setser, Hong Zhao, Journal of Clinical Investigation	2004	200
Peroxisome Proliferator–Activated Receptor-α Agonist Treatment in a Transgenic Model of Type 2 Diabetes Reverses the Lipotoxic State and Improves Glucose Homeostasis Hyunsook Kim, Martin Haluzı́k, Daphne Yau, Diabetes	2003	188
Genetic Background (C57BL/6J Versus FVB/N) Strongly Influences the Severity of Diabetes and Insulin Resistance in ob/ob Mice Martin Haluzı́k, Carlo Colombo, Oksana Gavrilova, Endocrinology Metabolic DisorderGeneticsGenetic EpidemiologyInsulin SignalingObesity	2004	178
Increased Tumor Growth in Mice with Diet-Induced Obesity: Impact of Ovarian Hormones Shoshana Yakar, Nomelí P. Núñez, P. Pennisi, Endocrinology PathologyGynecologyTumor BiologyOvarian CancerObesity	2006	151
Essential role of tyrosine residues 1131, 1135, and 1136 of the insulin-like growth factor-I (IGF-I) receptor in IGF-I action. H. Kato, Teresa N. Faria, Bethel Stannard, Molecular Endocrinology Insulin ReceptorInsulin SignalingSignaling PathwayIgf-i ActionReceptor Tyrosine Kinase	1994	145
Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplasia in skeletal muscle Ana M. Fernández, Joëlle Dupont, Roger P. Farrar, Journal of Clinical Investigation Muscle FunctionHuman GrowthCell CycleCell GrowthCellular Physiology	2002	133
Experimental Diabetes Increases Insulinlike Growth Factor I and II Receptor Concentration and Gene Expression in Kidney Haim Werner, Zila Shen‐Orr, Bethel Stannard, Diabetes Insulinlike Growth FactorRenal InflammationIgf-i ReceptorInsulin SignalingIi Receptor Concentration	1990	113

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