Lee S Weinstein

Metabolic Diseases Branch, NIDDK/NIH, United States of America

Lee S Weinstein is Chief of the Signal Transduction Section, Metabolic Diseases Branch, NIDDK, NIH.

His clinical interests are primarily in the areas of bone and mineral metabolism, with particular focus on hypocalcemic disorders and disorders of hormone resistance. His research primarily focuses on the role of G protein genetic and imprinting defects in human disease and the regulation and physiological roles of the imprinted GNAS gene.

Dr Weinstein is a member of the American Society of Bone and Mineral Research, American Society for the Advancement of Science, Endocrine Society, and American Society of Clinical Investigation and is on the Editorial Boards of Journal of Clinical Endocrinology and Metabolism and Clinical Cases in Mineral and Bone Metabolism.

Any competing interests declared are displayed with individual evaluations.

Faculty Member: Diabetes & Endocrinology > Bone & Mineral Metabolism (since 14 November 2005)

All recent recommendations

• 3.0
  A maternal epimutation of GNAS leads to Albright osteodystrophy and parathyroid hormone resistance.
  Recommended by Lee Weinstein
  
• 3.0
  Parathyroid hormone inhibits renal phosphate transport by phosphorylation of serine 77 of sodium-hydrogen exchanger regulatory factor-1.
  Recommended by Lee Weinstein
  
• 3.2
  The parathyroid is a target organ for FGF23 in rats.
  Recommended by Daniel Bikle, Lee Weinstein
  
• 3.0
  Aberrant Phex function in osteoblasts and osteocytes alone underlies murine X-linked hypophosphatemia.
  Recommended by Lee Weinstein
  
• 3.0
  Medical observation, compared with parathyroidectomy, for asymptomatic primary hyperparathyroidism: a prospective, randomized trial.
  Recommended by Lee Weinstein
  
• 6.0
  Normocalcemic primary hyperparathyroidism: further characterization of a new clinical phenotype.
  Recommended by Lee Weinstein
  
• 3.0
  Ruling out a suspect: the role of beta-catenin mutation in benign parathyroid neoplasia.
  Recommended by Lee Weinstein
  
• 3.0
  Adult hypophosphatasia treated with teriparatide.
  Recommended by Lee Weinstein
  
• 3.0
  Vitamin D receptor in chondrocytes promotes osteoclastogenesis and regulates FGF23 production in osteoblasts.
  Recommended by Lee Weinstein
  
• 9.0
  Hypothalamic mTOR signaling regulates food intake.
  Recommended by Lee Weinstein
  
• 3.0
  Activating mutations of the stimulatory g protein in juvenile ovarian granulosa cell tumors: a new prognostic factor?
  Recommended by Lee Weinstein
  
• 6.4
  FSH directly regulates bone mass.
  Recommended by Lee Weinstein, Carol Pilbeam
  
• 3.0
  Divergence of melanocortin pathways in the control of food intake and energy expenditure.
  Recommended by Lee Weinstein
  
• 3.0
  NFAT and Osterix cooperatively regulate bone formation.
  Recommended by Lee Weinstein
  
• 3.2
  SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis.
  Recommended by Alan Yu, Lee Weinstein