• KOL
    • Multiple Endocrine
    • William F Simonds
    • William F Simonds: Influence Statistics

      William F Simonds

      William F Simonds

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      National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD | National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, ...

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      William F Simonds:Expert Impact

      Concepts for whichWilliam F Simondshas direct influence:Multiple endocrine,Nuclear localization,Parathyroid cancer,Beta gamma,Adenylyl cyclase,Primary hyperparathyroidism,Lipid rafts,Nhe3 activity.

      William F Simonds:KOL impact

      Concepts related to the work of other authors for whichfor which William F Simonds has influence:Protein kinase,Primary hyperparathyroidism,Parathyroid carcinoma,Multiple endocrine,Adenylyl cyclase,Muscarinic receptor,Signal transduction.

      KOL Resume for William F Simonds

      Year
      2022

      National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD

      2021

      Metabolic Diseases Branch, Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA

      2020

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Disease (NIDDK)

      2019

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA

      2018

      Metabolic Disease Branch, National Institutes of Digestive Disease and Kidney, National Institutes of Health, Bethesda, MD.

      2017

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. Dr. Loshakov is now with the The Commonwealth Medical College, Scranton, PA, USA and Dr. Sholevar is now with the Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.

      The National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892

      2016

      National Institutes of HealthBethesda, Maryland, USA

      2015

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD

      2014

      Metabolic Diseases Branch, National Institute of Digestive and Diabetes and Kidney Diseases, National Institutes of Health, Bethesda, MD

      2012

      Metabolic Diseases Branch (L.S.W., W.F.S., S.J.M.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892

      2011

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

      2010

      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

      2009

      Metabolic Diseases Branch, NIDDK, Bethesda, MD

      2008

      National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA

      2007

      Metabolic Diseases Branch, 10/8C-101, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA

      2006

      National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

      2005

      Metabolic Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, 20892, Bethesda, MD, USA

      Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-1802

      2004

      Metabolic Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 20892, Bethesda, MD, USA

      2003

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892-1752, USA.

      2002

      From Metabolic Diseases Branch (WFS, LAJ-N, SKA, MCS, SJM), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, and Departments of Medicine, Physiology and Human Genetics (BY, GNH), McGill University, and Calcium Research Laboratory, Royal Victoria Hospital, Montreal, Quebec, Canada.

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, USA

      2001

      Metabolic Diseases Branch, NIDDK, Bethesda, Maryland 20892-1752

      National Research Laboratory for the Study of Ginseng Signal Transduction and Department of Physiology, College of Veterinary Medicine, Chonnam National University, Kwangju 500-757 Korea

      Bethesda, Md, New York, NY, San Francisco, Calif, and Philadelphia, Pa

      2000

      Metabolic Diseases Branch, Bldg. 10, Room 8C-101, 10 Center Dr., MSC 1752, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA

      1999

      Metabolic Diseases Branch/NIDDK National Institutes of Health Bldg 10/ Room 8C-101, 10 CENTER DR. MSC 1752, Bethesda, MD 20892-1752, USA.

      1998

      Department of Physiological Chemistry II, University of Düsseldorf, Düsseldorf, D‐40225, Germany

      1997

      MDB/NIDDK, National Institutes of Health, Bethesda, Maryland 20892-1752

      1996

      Metabolic Diseases Branch, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, 20892, Bethesda, Maryland

      1995

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA

      1994

      Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 20892, Bethesda, Maryland, USA

      1993

      Molecular Pathophysiology Branch, National Institutes of Diabetes, Digestive and Kidney Diseases, Bethesda, MD 20892.

      1992

      Molecular Pathophysiology Section, Metabolic Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 USA

      1991

      Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, USA

      Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

      1990

      Molecular Pathophysiology Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, 20892, Bethesda, Md., USA

      Laboratory of General and Comparative Biochemistry, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892.

      1989

      Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.

      1988

      Molecular Pathophysiology Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, Bethesda, Maryland 20892

      1985

      Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, MD 20205, U.S.A

      1984

      Laboratory of General and Comparative Biochemistry, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20205, USA

      1982

      Laboratory of General and Comparative Biochemistry, NIMH, National Institutes of Health, Bethesda, MD 20205, USA

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      Sample of concepts for which William F Simonds is among the top experts in the world.
      Concept World rank
      encoded hrpt2 #1
      rmhlrqyell #1
      akt1s1 pras40 #1
      mediated gsalpha #1
      activation effector pathways #1
      expression gbeta5long #1
      parafibromin l95p #1
      iopthresultsthirty patients #1
      localization beta5 #1
      jnk phospholipase #1
      inhibitor treatment menorrhagia #1
      gamma glugluphe #1
      beta5 r7 #1
      nuclear fraction rgs7 #1
      suggestion solubilized receptors #1
      patients seemingly sporadic #1
      signals erks #1
      mutation parafibromin #1
      hrpt2 fihp #1
      effector pathways mapk #1
      xlms proteins structureactivity #1
      unpredictable efficiency #1
      e10k mutation #1
      multistep process ras #1
      beta gamma cdnas #1
      cbeta2 activation #1
      cyclaseforskolin complex #1
      tight physiologic range #1
      rgs r7bp #1
      cyclase catalytic core #1
      binding toβγ #1
      adenylylcyclase cell types #1
      impeding issues #1
      55 kda gbeta5 #1
      hpt manifestation #1
      gbeta5 nuclear expression #1
      hptjt menorrhagia ovulation #1
      parafibromin function #1
      expression heterotrimeric #1
      defective nucleolar #1
      secondary nls #1
      parathyroid hpt #1
      expression parafibromin #1
      gbeta5 nucleus cytosol #1
      hpt neoplasia #1
      nuclear beta5 #1
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      Prominent publications by William F Simonds

      KOL-Index: 14166

      While positive regulation of c-Akt (also known as protein kinase B) by receptor tyrosine kinases is well documented, compounds acting through G protein-coupled receptors can also activate Akt and its downstream targets. We therefore explored the role of G protein subunits in the regulation of Akt in cultured mammalian cells. In HEK-293 and COS-7 cells transiently transfected with beta(2)-adrenergic or m2 muscarinic receptors, respectively, treatment with agonist-induced phosphorylation ...

      Known for Protein Kinase | Activation Akt | Muscarinic Receptors | Gtp Binding | Cos Cells
      KOL-Index: 12779

      The role that Gbeta(5) regulator of G protein signaling (RGS) complexes play in signal transduction in brain remains unknown. The subcellular localization of Gbeta(5) and RGS7 was examined in rat PC12 pheochromocytoma cells and mouse brain. Both nuclear and cytosolic localization of Gbeta(5) and RGS7 was evident in PC12 cells by immunocytochemical staining. Subcellular fractionation of PC12 cells demonstrated Gbeta(5) immunoreactivity in the membrane, cytosolic, and nuclear fractions. ...

      Known for Nuclear Localization | Protein Β5 | Gbeta5 Rgs7 | Pc12 Cells | Neurons Brain
      KOL-Index: 12295

      NHE3 activity is regulated by phosphorylation/dephosphorylation processes and membrane recycling in intact cells. However, the Na(+)/H(+) exchanger (NHE) can also be regulated by G proteins independent of cytoplasmic second messengers, but the G protein subunits involved in this regulation are not known. Therefore, we studied G protein subunit regulation of NHE3 activity in renal brush-border membrane vesicles (BBMV) in a system devoid of cytoplasmic components and second messengers. ...

      Known for Nhe3 Activity | Protein Subunits | Gtp Binding | Inbred Wky Receptors | Renal Brush
      KOL-Index: 12254

      Familial hyperparathyroid syndromes involving mutations of HRPT2 (also CDC73), a tumor suppressor, are important to identify because the relatively high incidence of parathyroid malignancy associated with such mutations warrants a specific surveillance strategy. However, there is a dearth of reports describing experience with surveillance and early detection informed by genetic insight into this disorder.

      INTRODUCTION: Familial isolated hyperparathyroidism (FIHP) is a rare cause of ...

      Known for Hrpt2 Mutation | Atypical Adenoma | Primary Hyperparathyroidism | Familial Isolated | Tumor Suppressor
      KOL-Index: 11746

      Genetic evidence suggests that the yeast STE4 and STE18 genes encode G beta and G gamma subunits, respectively, that the G betagamma complex plays a positive role in the pheromone response pathway, and that its activity is subject to negative regulation by the G alpha subunit (product of the GPA1 gene) and to positive regulation by cell-surface pheromone receptors. However, as yet there is no direct biochemical evidence for a G betagamma protein complex associated with the plasma ...

      Known for Plasma Membrane | Pheromone Response | Binding Protein | Ste4p Ste18p | Subunits Gtp
      KOL-Index: 11716

      Stimulation of a variety of cell surface receptors enhances the enzymatic activity of mitogen-activated protein kinases (MAPKs). MAPKs have been classified in three subfamilies: extracellular signal-regulated kinases (ERKs), stress-activated protein kinases or c-Jun NH2-terminal kinases (SAPKs/JNKs), and p38 kinase. Whereas the pathway linking cell surface receptors to ERKs has been partially elucidated, the mechanism of activation of JNKs is still poorly understood. Recently, we have ...

      Known for Coupled Receptors | Jnk Stimulation | Heterotrimeric Proteins | Jun Kinase | Signaling Pathway
      KOL-Index: 10945

      CONTEXT: One variant of multiple endocrine neoplasia type 1 (MEN1) is defined by sporadic tumors of both the parathyroids and pituitary. 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.

      OBJECTIVE: The objective was to test p27 in germline DNA from cases with tumors of both the parathyroids and pituitary.

      DESIGN: Medical ...

      Known for Multiple Endocrine | Neoplasia Type | Germline Mutation | P27 Gene | Sporadic Tumors
      KOL-Index: 10441

      BACKGROUND: Heterotrimeric guanine nucleotide-binding regulatory proteins (G proteins), composed of G alpha, G beta, and G gamma subunits, are positioned at the inner face of the plasma membrane and relay signals from activated G protein-coupled cell surface receptors to various signaling pathways. G beta 5 is the most structurally divergent G beta isoform and forms tight heterodimers with regulator of G protein signalling (RGS) proteins of the R7 subfamily (R7-RGS). The subcellular ...

      Known for Lipid Rafts | Binding Protein | R7 Rgs | Neurons Brain | Pc12 Cells
      KOL-Index: 10283

      Abstract MITOGEN-ACTIVATED protein kinases, MAP kinases or ERKs (extracellular signal-regulated kinases) are rapidly stimulated by growth-promoting factors acting on a variety of cell-surface receptors1,2. In turn, ERKs phosphorylate and regulate key intra-cellular enzymes and transcription factors involved in the control of cellular proliferation3,4. The tyrosine-kinase class of growth-factor receptors transmits signals to ERKs in a multistep process that involves Ras and a limited ...

      Known for Map Kinase Pathway | Erk Activation | Protein Βγ | Muscarinic Receptors | Adenylyl Cyclase
      KOL-Index: 10015

      The expression and assembly of particular combinations of beta and gamma subunit isoforms into beta gamma heterodimers may contribute to the specificity of signal transduction mediated by heterotrimeric guanine nucleotide binding regulatory proteins. Using a transient transfection paradigm to examine selectivity in beta gamma heterodimer formation, we find that gamma 1 interacts with beta 1 but not with beta 2, while both beta subunits interact with gamma 2 and that a beta 2/beta 1 ...

      Known for Beta Gamma | Multiple Domains | Signal Transduction | Heterotrimeric Guanine | Binding Proteins
      KOL-Index: 9869

      We report here the identification of a gene associated with the hyperparathyroidism–jaw tumor (HPT–JT) syndrome. A single locus associated with HPT–JT (HRPT2) was previously mapped to chromosomal region 1q25–q32. We refined this region to a critical interval of 12 cM by genotyping in 26 affected kindreds. Using a positional candidate approach, we identified thirteen different heterozygous, germline, inactivating mutations in a single gene in fourteen families with HPT–JT. The proposed ...

      Known for Jaw Tumor | Encoding Parafibromin | Suppressor Proteins | Gene Hyperparathyroidism | Mutation Screening
      KOL-Index: 9783

      While multiple G protein beta and gamma subunit isoforms have been identified, the implications of this potential diversity of betagamma heterodimers for signaling through betagamma-regulated effector pathways remains unclear. Furthermore the molecular mechanism(s) by which the betagamma complex modulates diverse mammalian effector molecules is unknown. Effector signaling by the structurally distinct brain-specific beta5 subunit was assessed by transient cotransfection with gamma2 in COS ...

      Known for Effector Pathways | Cos Cells | Beta5 Gamma2 | Gtp Binding | Protein Beta
      KOL-Index: 9712

      Parafibromin is the 531-amino-acid protein product encoded by HRPT2, a putative tumor suppressor gene recently implicated in the autosomal dominant hyperparathyroidism–jaw tumor familial cancer syndrome, sporadic parathyroid cancer, and a minority of families with isolated hyperparathyroidism. Parafibromin contains no identified functional domains but bears sequence homology to Cdc73p, a budding yeast protein component of the RNA polymerase II-associated Paf1 complex. This study ...

      Known for Cyclin D1 | Expression Parafibromin | Jaw Tumor | Parathyroid Cancer | Carcinoma Cell
      KOL-Index: 9657

      We transfected COS cells with cDNAs for the alpha subunits of stimulatory and inhibitory GTP-binding proteins, alpha s and alpha i1, respectively, and immunoprecipitated the metabolically labeled products with specific peptide antibodies. Cells were separated into particulate and soluble fractions before immunoprecipitation; [35S]methionine-labeled alpha s and alpha i were both found primarily in the particulate fraction. [3H]Myristate was incorporated into endogenous and transfected ...

      Known for Membrane Attachment | Protein Alpha | Cos Cells | Particulate Fraction | Adenosine Diphosphate

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      National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD | National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA;, bills@niddk.nih.gov | Metabolic Diseases Branch, Metabolic Diseases Bran

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