William F. Simonds
National Institutes of Health
141 Papers
1.6K Citations
William F. Simonds is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Hyperparathyroidism & Medicine. The author has an hindex of 46, co-authored 124 publications.
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Papers
Identification of a Mr 58 000 glycoprotein subunit of the opiate receptor
Werner A. Klee,William F. Simonds,Floyd W. Sweat,Terrence R. Burke,Arthur E. Jacobson,Kenner C. Rice +5 more
TL;DR: A M r 58 000 subunit of the opiate receptor has been identified using tritiated fentanyl isothiocyanate, a potent opiate alkylating reagent with specificity for the δ‐opiate receptor subclass.
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Nuclear Localization of G Protein β5 and Regulator of G Protein Signaling 7 in Neurons and Brain
Jian-Hua Zhang,Valarie A. Barr,Yinyuan Mo,Alexandra M. Rojkova,Shaohua Liu,William F. Simonds +5 more
TL;DR: It is suggested that Gβ5 undergoes nuclear translocation in neurons via an RGS-dependent mechanism and the novel intracellular distribution of G β5·RGS protein complexes suggests a potential role in neurons communicating between classical heterotrimeric G protein subunits and/or their effectors at the plasma membrane and the cell nucleus.
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Multiple Endocrine Neoplasia Type 1 Variant with Frequent Prolactinoma and Rare Gastrinoma
Wei Hao,Monica C. Skarulis,William F. Simonds,Lee S. Weinstein,Sunita K. Agarwal,Carmen M. Mateo,Laura James-Newton,Gerald R. Hobbs,Fathia Gibril,Robert T. Jensen,Stephen J. Marx +10 more
TL;DR: This variant of multiple endocrine neoplasia type 1 shows more frequent prolactinoma and less frequent gastrinoma than typical MEN1; the variant is reproducible among kindreds.
Impaired cotranslational processing of the calcium-sensing receptor due to signal peptide missense mutations in familial hypocalciuric hypercalcemia
TL;DR: This is the first study examining the function of the CASR signal sequence and reveals that both L11S and L13P mutants are markedly impaired with respect to cotranslational processing, accounting for the observed parathyroid dysfunction.
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Nuclear Localization of the Parafibromin Tumor Suppressor Protein Implicated in the Hyperparathyroidism-Jaw Tumor Syndrome Enhances Its Proapoptotic Function
TL;DR: These experiments identify for the first time a proapoptotic activity of endogenous parafibromin likely to be important in its role as a tumor suppressor and show a functional role for the NLS of parafIBromin in this activity.
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