William F Simonds

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint G protein-regulated signaling dysfunction in human disease
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 1752, USA
    J Investig Med 51:194-214. 2003
  2. pmc Cushing's syndrome in multiple endocrine neoplasia type 1
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
    Clin Endocrinol (Oxf) 76:379-86. 2012
  3. ncbi request reprint Selective activation of effector pathways by brain-specific G protein beta5
    S Zhang
    Metabolic Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 271:33575-9. 1996
  4. ncbi request reprint Familial isolated hyperparathyroidism: clinical and genetic characteristics of 36 kindreds
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Medicine (Baltimore) 81:1-26. 2002
  5. ncbi request reprint New dimensions in G protein signalling: G beta 5 and the RGS proteins
    W F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Pharm Acta Helv 74:333-6. 2000
  6. ncbi request reprint Parafibromin, product of the hyperparathyroidism-jaw tumor syndrome gene HRPT2, regulates cyclin D1/PRAD1 expression
    Geoffrey E Woodard
    1Metabolic Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Oncogene 24:1272-6. 2005
  7. pmc Sleeping parathyroid tumor: rapid hyperfunction after removal of the dominant tumor
    Sahzene Yavuz
    Diabetes, Endocrine and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 97:1834-41. 2012
  8. pmc Nuclear localization of the G protein beta 5/R7-regulator of G protein signaling protein complex is dependent on R7 binding protein
    Leelamma M Panicker
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1752, USA
    J Neurochem 113:1101-12. 2010
  9. ncbi request reprint Familial isolated hyperparathyroidism is rarely caused by germline mutation in HRPT2, the gene for the hyperparathyroidism-jaw tumor syndrome
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 89:96-102. 2004
  10. pmc Reoperation for parathyroid adenoma: a contemporary experience
    Anathea C Powell
    Tumor Angiogenesis Section, Surgery Branch, NCI, Bethesda, MD, USA
    Surgery 146:1144-55. 2009

Collaborators

Detail Information

Publications37

  1. ncbi request reprint G protein-regulated signaling dysfunction in human disease
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 1752, USA
    J Investig Med 51:194-214. 2003
  2. pmc Cushing's syndrome in multiple endocrine neoplasia type 1
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
    Clin Endocrinol (Oxf) 76:379-86. 2012
    ..The purpose of this study was to characterize the range of presentations of CS in a large series of MEN1 patients...
  3. ncbi request reprint Selective activation of effector pathways by brain-specific G protein beta5
    S Zhang
    Metabolic Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 271:33575-9. 1996
    ....
  4. ncbi request reprint Familial isolated hyperparathyroidism: clinical and genetic characteristics of 36 kindreds
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    Medicine (Baltimore) 81:1-26. 2002
  5. ncbi request reprint New dimensions in G protein signalling: G beta 5 and the RGS proteins
    W F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Pharm Acta Helv 74:333-6. 2000
    ..These recent novel observations further reinforce the view of G beta 5 as a unique and highly specialized G protein subunit...
  6. ncbi request reprint Parafibromin, product of the hyperparathyroidism-jaw tumor syndrome gene HRPT2, regulates cyclin D1/PRAD1 expression
    Geoffrey E Woodard
    1Metabolic Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Oncogene 24:1272-6. 2005
    ..These results demonstrate that human parafibromin is a nucleocytoplasmic protein with functions consistent with its postulated role as a tumor suppressor protein...
  7. pmc Sleeping parathyroid tumor: rapid hyperfunction after removal of the dominant tumor
    Sahzene Yavuz
    Diabetes, Endocrine and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 97:1834-41. 2012
    ..A fall of intraoperative serum PTH by a certain percentage during parathyroid surgery is often used as one criterion for ending the operation...
  8. pmc Nuclear localization of the G protein beta 5/R7-regulator of G protein signaling protein complex is dependent on R7 binding protein
    Leelamma M Panicker
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1752, USA
    J Neurochem 113:1101-12. 2010
    ..These results suggest that R7BP contributes significantly to the nuclear localization of endogenous G beta(5)/R7-RGS complex in brain...
  9. ncbi request reprint Familial isolated hyperparathyroidism is rarely caused by germline mutation in HRPT2, the gene for the hyperparathyroidism-jaw tumor syndrome
    William F Simonds
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 89:96-102. 2004
    ..Even accounting for families with one of the three occult syndromes and false negative biochemical or DNA testing, these results indicate that an unexpectedly large fraction of FIHP has currently unrecognized causes...
  10. pmc Reoperation for parathyroid adenoma: a contemporary experience
    Anathea C Powell
    Tumor Angiogenesis Section, Surgery Branch, NCI, Bethesda, MD, USA
    Surgery 146:1144-55. 2009
    ..We reviewed reoperations for persistent or recurrent sporadic parathyroid adenoma to evaluate and compare our current results and outcomes to our previous experience...
  11. pmc Defective nucleolar localization and dominant interfering properties of a parafibromin L95P missense mutant causing the hyperparathyroidism-jaw tumor syndrome
    Leelamma M Panicker
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 10, Room 8C 101, Bethesda, Maryland 20892, USA
    Endocr Relat Cancer 17:513-24. 2010
    ....
  12. ncbi request reprint Hyperparathyroidism in hereditary syndromes: special expressions and special managements
    Stephen J Marx
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 1802, USA
    J Bone Miner Res 17:N37-43. 2002
    ..The CASR test, perhaps least urgent, has largely been unavailable. Further progress in molecular genetics will enhance understandings, diagnosis, and therapy of HPT...
  13. doi request reprint Utility of intraoperative parathyroid hormone monitoring in patients with multiple endocrine neoplasia type 1-associated primary hyperparathyroidism undergoing initial parathyroidectomy
    Naris Nilubol
    Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, MSC1201 Room 3 3940, Bethesda, MD 20892 1201, USA
    World J Surg 37:1966-72. 2013
    ..Intraoperative parathyroid hormone monitoring (IOPTH) is a widely used adjunct for primary hyperparathyroidism (pHPT). However, the benefit of IOPTH in familial pHPT, such as in multiple endocrine neoplasia type I (MEN1), remains unclear...
  14. pmc Association of type-O blood with neuroendocrine tumors in multiple endocrine neoplasia type 1
    Allison B Weisbrod
    Endocrine Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 98:E109-14. 2013
    ..We recently reported an association between O blood type and the manifestation of pancreatic neuroendocrine tumors in a cohort of patients with Von Hippel-Lindau syndrome...
  15. ncbi request reprint Multiple endocrine neoplasia type 1 variant with frequent prolactinoma and rare gastrinoma
    Wei Hao
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Endocrinol Metab 89:3776-84. 2004
    ..MEN1 carriers in such families should have periodic monitoring adjusted for the expected penetrance of tumors...
  16. ncbi request reprint Nuclear localization of the parafibromin tumor suppressor protein implicated in the hyperparathyroidism-jaw tumor syndrome enhances its proapoptotic function
    Ling Lin
    Metabolic Diseases Branch National Institutes of Diabetes, Digestive and Kidney Diseases, NIH, Room 8C 101, Building 10, 10 Center Drive, MSC 1752, Bethesda, MD 20892 1752, USA
    Mol Cancer Res 5:183-93. 2007
    ..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...
  17. ncbi request reprint The parathyroid/pituitary variant of multiple endocrine neoplasia type 1 usually has causes other than p27Kip1 mutations
    Atsushi Ozawa
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1802, USA
    J Clin Endocrinol Metab 92:1948-51. 2007
    ..The prevalence of identified MEN1 mutations in this variant is lower than in familial MEN1 (7% vs. 90%), suggesting different causes. Recently, one case of this variant had a germline mutation of p27(Kip1)/CDKN1B...
  18. pmc The parafibromin tumor suppressor protein interacts with actin-binding proteins actinin-2 and actinin-3
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA
    Mol Cancer 7:65. 2008
    ..HRPT2 encodes parafibromin. To identify parafibromin interacting proteins we used the yeast two-hybrid system for screening a heart cDNA library with parafibromin as the bait...
  19. doi request reprint Preoperative localizing studies for initial parathyroidectomy in MEN1 syndrome: is there any benefit?
    Naris Nilubol
    Endocrine Oncology Section, Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, MSC1201 Rm 3 3940, Bethesda, MD 20892 1201, USA
    World J Surg 36:1368-74. 2012
    ..The objective of the present study was to evaluate the utility of preoperative localizing studies in patients with MEN1 undergoing initial bilateral neck exploration (BNE) and parathyroidectomy for pHPT...
  20. ncbi request reprint Utility of rapid intraoperative parathyroid hormone assay to predict severe postoperative hypocalcemia after reoperation for hyperparathyroidism
    Dina M Elaraj
    Surgery Branch, National Cancer Institute, Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases NIH, Building 10, Room 2B07, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Surgery 132:1028-33; discussion 1033-4. 2002
    ..This study's purpose was to determine the utility of intraoperative parathyroid hormone (IO-PTH) values in predicting the development of severe hypocalcemia for patients undergoing reoperation for primary hyperparathyroidism...
  21. pmc The parafibromin tumor suppressor protein inhibits cell proliferation by repression of the c-myc proto-oncogene
    Ling Lin
    Metabolic Diseases Branch, Building 10 Room 8C 101, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 105:17420-5. 2008
    ..These experiments provide a previously uncharacterized mechanism for the anti-proliferative action of the parafibromin tumor suppressor protein resulting from PAF1 complex-mediated inhibition of the c-myc proto-oncogene...
  22. pmc R7-binding protein targets the G protein beta 5/R7-regulator of G protein signaling complex to lipid rafts in neuronal cells and brain
    Lylia Nini
    Metabolic Diseases Branch, 10 8C 101, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    BMC Biochem 8:18. 2007
    ....
  23. ncbi request reprint Assays of nuclear localization of R7/Gbeta5 complexes
    William F Simonds
    Metabolic Diseases Branch NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    Methods Enzymol 390:210-23. 2004
    ....
  24. pmc Clinical and molecular genetics of parathyroid neoplasms
    John M Sharretts
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg 10 Room 8C 101, 10 Center Dr MSC 1752 Bethesda, MD 20892 1752, USA
    Best Pract Res Clin Endocrinol Metab 24:491-502. 2010
    ..Studies of familial isolated HPT and analysis of chromosomal loss and gain in parathyroid tumours suggest that other genes relevant to parathyroid neoplasia await identification...
  25. ncbi request reprint HRPT2, a marker of parathyroid cancer
    Lee S Weinstein
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, USA
    N Engl J Med 349:1691-2. 2003
  26. ncbi request reprint Ggamma subunit-selective G protein beta 5 mutant defines regulators of G protein signaling protein binding requirement for nuclear localization
    Alexandra M Rojkova
    Metabolic Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 278:12507-12. 2003
    ..The Ggamma-selective Gbeta(5) mutant was also excluded from the cell nucleus of transfected PC12 cells analyzed by laser confocal microscopy. These results define a requirement for RGS protein binding for Gbeta(5) nuclear expression...
  27. pmc Parathyroid cancer
    John M Sharretts
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1752, USA
    Semin Oncol 37:580-90. 2010
    ..Metastatic disease can be palliated with surgical debulking. Medical therapy with the calcimimetic cinacalcet and bisphosphonates can ameliorate hypercalcemia in patients with inoperable disease...
  28. ncbi request reprint Molecular pathology of the MEN1 gene
    Sunita K Agarwal
    National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 1014:189-98. 2004
    ..The Men1+/- mouse has robust MEN1; its most important difference from human MEN1 is marked hyperplasia of pancreatic islets, a tumor precursor stage...
  29. pmc Aromatase inhibitor treatment of menorrhagia and subsequent pregnancy in a patient with familial hyperparathyroidism-jaw tumor syndrome
    Erin F Wolff
    Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland, USA
    Fertil Steril 98:1616-9. 2012
    ..To describe the clinical management of menorrhagia in a woman with hyperparathyroidism-jaw tumor syndrome (HPT-JT)...
  30. pmc Knockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice
    Jian Hua Zhang
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
    J Neurochem 119:544-54. 2011
    ..Taken together with previous observations from Gnb5 KO mice, our findings suggest a model in which Gβ5 regulates dendritic arborization and/or synapse formation during development, in part by effects on gene expression...
  31. ncbi request reprint Hereditary hormone excess: genes, molecular pathways, and syndromes
    Stephen J Marx
    Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases NIH, Building 10, Room 9C 101, 10 Center Drive, MSC 1802, Bethesda, MD 20892 1802, USA
    Endocr Rev 26:615-61. 2005
    ..In many cases, monoclonal proliferation causes hormone excess, probably as a secondary consequence of accumulation of cells with coincidental hormone-secretory ability...
  32. ncbi request reprint Editorial: Imaging to detect early endocrine cancers
    Stephen J Marx
    J Clin Endocrinol Metab 91:2861-3. 2006
  33. ncbi request reprint Impaired cotranslational processing of the calcium-sensing receptor due to signal peptide missense mutations in familial hypocalciuric hypercalcemia
    Svetlana Pidasheva
    Department of Medicine, McGill University, Montreal, Quebec, Canada
    Hum Mol Genet 14:1679-90. 2005
    ..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...
  34. ncbi request reprint Surveillance for early detection of aggressive parathyroid disease: carcinoma and atypical adenoma in familial isolated hyperparathyroidism associated with a germline HRPT2 mutation
    Thomas G Kelly
    Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06520 8064, USA
    J Bone Miner Res 21:1666-71. 2006
    ..However, there is a dearth of reports describing experience with surveillance and early detection informed by genetic insight into this disorder...
  35. ncbi request reprint Ruling out a suspect: the role of beta-catenin mutation in benign parathyroid neoplasia
    William F Simonds
    J Clin Endocrinol Metab 92:1235-6. 2007
  36. ncbi request reprint Adenylyl cyclase type-VIII activity is regulated by G(betagamma) subunits
    Debora Steiner
    Department of Neurobiology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Cell Signal 18:62-8. 2006
    ..These results demonstrate that Gbetagamma (originating from agonist activation of these receptors) and probably not Galphai/o subunits are involved in the agonist inhibition of AC-VIII...
  37. ncbi request reprint topors, a p53 and topoisomerase I-binding RING finger protein, is a coactivator of p53 in growth suppression induced by DNA damage
    Ling Lin
    Department of Molecular Embryology, Graduate School of Medicine, Chiba University, 1 8 1 Inohana, Chuo Ku, Chiba 260 8670, Japan
    Oncogene 24:3385-96. 2005
    ..We therefore postulate that topors mediates p53-dependent cellular responses induced by DNA damage, suggesting its physiological role as a tumor suppressor...