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Biology and Biochemistry

D-Index
52
Citations
10768
World Ranking
16611
National Ranking
6871

Overview

William F. Simonds is affiliated with the National Institutes of Health in the United States. Their research primarily spans the fields of medicine and biochemistry, genetics, and molecular biology, with a significant focus on nephrology, genetics, oncology, epidemiology, and neurology.

Their scholarly output covers a variety of topics, including the following areas:

  • Parathyroid Disorders and Treatments
  • Neuroendocrine Tumor Research Advances
  • Genetic Syndromes and Imprinting
  • Neuroblastoma Research and Treatments
  • Pancreatic and Hepatic Oncology Research
  • Soft tissue tumor case studies
  • Medical Imaging and Pathology Studies

William F. Simonds has contributed to numerous papers, several of which were published in prominent journals. Recent notable publications include:

  • "Molecular and Clinical Spectrum of Primary Hyperparathyroidism," 2023, Endocrine Reviews
  • "Parathyroid Carcinoma: Incidence, Survival Analysis, and Management: A Study from the SEER Database and Insights into Future Therapeutic Perspectives," 2022, Cancers
  • "Genotype of CDC73 germline mutation determines risk of parathyroid cancer," 2020, Endocrine Related Cancer
  • "Familial Hyperparathyroidism," 2021, Frontiers in Endocrinology
  • "Phenotypic Profiling and Molecular Mechanisms in Hyperparathyroidism-jaw Tumor Syndrome," 2023, The Journal of Clinical Endocrinology & Metabolism

Coauthor collaborations are a significant component of their work. Frequent collaborators include Lee S. Weinstein, Sunita Agarwal, Smita Jha, James Welch, and Jenny E. Blau.

William F. Simonds has published extensively in specific journals, which include:

  • Journal of the Endocrine Society
  • The Journal of Clinical Endocrinology & Metabolism
  • Endocrine Related Cancer
  • Frontiers in Endocrinology
  • JCI Insight

Best Publications

  • Ras-dependent activation of MAP kinase pathway mediated by G-protein βγ subunits

    P. Crespo;Ningzhi Xu;W. F. Simonds;J. S. Gutkind

  • HRPT2, encoding parafibromin, is mutated in hyperparathyroidism–jaw tumor syndrome

    J.D. Carpten;C.M. Robbins;A. Villablanca;L. Forsberg

  • Gi2 mediates alpha 2-adrenergic inhibition of adenylyl cyclase in platelet membranes: in situ identification with G alpha C-terminal antibodies.

    William F. Simonds;Paul K. Goldsmith;Juan Codina;Cecilia G. Unson

  • Signaling from G protein-coupled receptors to c-Jun kinase involves beta gamma subunits of heterotrimeric G proteins acting on a Ras and Rac1-dependent pathway.

    Omar A. Coso;Hidemi Teramoto;William F. Simonds;J. Silvio Gutkind

  • G protein regulation of adenylate cyclase.

    William F. Simonds

  • Familial isolated hyperparathyroidism: clinical and genetic characteristics of 36 kindreds.

    William F. Simonds;Laura A. James-Newton;Sunita K. Agarwal;Bing Yang

  • Solubilization of active opiate receptors

    William F. Simonds;Greg Koski;Richard A. Streaty;Leonard M. Hjelmeland

  • Myristoylation of an inhibitory GTP-binding protein alpha subunit is essential for its membrane attachment.

    Teresa L. Z. Jones;William F. Simonds;John J. Merendino;Mark R. Brann

  • G-protein beta gamma dimers. Membrane targeting requires subunit coexpression and intact gamma C-A-A-X domain.

    W F Simonds;J E Butrynski;N Gautam;C G Unson

  • Multiple endocrine neoplasia type 1: new clinical and basic findings.

    Debra H Schussheim;Monica C Skarulis;Sunita K Agarwal;William F Simonds

  • Receptor and effector interactions of Gs Functional studies with antibodies to the αs carboxyl-terminal decapeptide

    William F. Simonds;Paul K. Goldsmith;Charles J. Woodard;Cecilia G. Unson

  • Familial isolated hyperparathyroidism is rarely caused by germline mutation in HRPT2, the gene for the hyperparathyroidism-jaw tumor syndrome.

    William F. Simonds;Christiane M. Robbins;Sunita K. Agarwal;Geoffrey N. Hendy

  • Identification of the GTP-binding protein encoded by Gi3 complementary DNA.

    P Goldsmith;K Rossiter;A Carter;W Simonds

  • Parafibromin, product of the hyperparathyroidism-jaw tumor syndrome gene HRPT2, regulates cyclin D1/PRAD1 expression.

    Geoffrey E Woodard;Ling Lin;Jian-Hua Zhang;Sunita K Agarwal

  • Molecular Pathology of the MEN1 Gene

    Sunita K. Agarwal;A. Lee Burns;Karen E. Sukhodolets;Patricia A. Kennedy

  • Hyperparathyroidism in hereditary syndromes: special expressions and special managements.

    Stephen J. Marx;William F. Simonds;Sunita K. Agarwal;A. Lee Burns

  • Clinical and molecular genetics of parathyroid neoplasms

    John M. Sharretts;William F. Simonds

  • The G protein connection: molecular basis of membrane association

    Allen M. Spiegel;Peter S. Backlund;James E. Butrynski;James E. Butrynski;Teresa L.Z. Jones

  • The parafibromin tumor suppressor protein inhibits cell proliferation by repression of the c-myc proto-oncogene.

    Ling Lin;Jian-Hua Zhang;Leelamma M. Panicker;William F. Simonds

  • Dual regulation of Akt/protein kinase B by heterotrimeric G protein subunits.

    Rajani K. Bommakanti;Shaveta Vinayak;William F. Simonds

Frequent Co-Authors

Stephen J. Marx
Stephen J. Marx National Institutes of Health
Allen M. Spiegel
Allen M. Spiegel Albert Einstein College of Medicine
Electron Kebebew
Electron Kebebew Stanford University
Steven K. Libutti
Steven K. Libutti Rutgers, The State University of New Jersey
Monica C. Skarulis
Monica C. Skarulis National Institutes of Health
Robert T. Jensen
Robert T. Jensen National Institutes of Health
Paul Goldsmith
Paul Goldsmith National Institutes of Health
H. Richard Alexander
H. Richard Alexander Rutgers, The State University of New Jersey
Arthur E. Jacobson
Arthur E. Jacobson National Institutes of Health
Terrence R. Burke
Terrence R. Burke National Institutes of Health

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