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Genomes and Genes | MONE contact ZAIDISummaryAffiliation: Mount Sinai School of Medicine Country: USA Publications
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Publications
Special stem cells for boneMone Zaidi
The Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Cell Stem Cell 10:233-4. 2012..In this issue of Cell Stem Cell, Park et al. (2012) report that an MSC-like, osteolineage-directed Mx1+ population generates new osteoblasts at sites of bone damage, suggesting its potential for skeletal repair and regeneration...- Bone loss or lost bone: rationale and recommendations for the diagnosis and treatment of early postmenopausal bone lossMone Zaidi
The Mount Sinai Bone Program, Box 1055, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
Curr Osteoporos Rep 7:118-26. 2009.... - New insights: elevated follicle-stimulating hormone and bone loss during the menopausal transitionMone Zaidi
The Mount Sinai Bone Program, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
Curr Rheumatol Rep 11:191-5. 2009..Potential therapeutic implications include the development of antagonists to circulating FSH and its osteoclastic receptor... 
Paradigm shift in the pathophysiology of postmenopausal and thyrotoxic osteoporosisMone Zaidi
Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY, USA
Mt Sinai J Med 76:474-83. 2009..New therapeutic targets thus emerge from these studies. Mt Sinai J Med 76:474-483, 2009. (c) 2009 Mount Sinai School of Medicine...- Thyroid-stimulating hormone, thyroid hormones, and bone lossMone Zaidi
Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA
Curr Osteoporos Rep 7:47-52. 2009..TSH and its receptor could become valuable drug targets in treating bone loss... - Skeletal remodeling in health and diseaseMone Zaidi
The Mount Sinai Bone Program, Department of Medicine, Box 1055, Mount Sinai School of Medicine, New York, New York 10029, USA
Nat Med 13:791-801. 2007..It also highlights molecular aberrations that cause bone cells to become dysfunctional, as well as therapeutic options and opportunities to counteract skeletal loss... 
ACTH protects against glucocorticoid-induced osteonecrosis of boneMone Zaidi
The Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 107:8782-7. 2010..We suggest examining the efficacy of ACTH in preventing human osteonecrosis, a devastating complication of glucocorticoid therapy...- New horizons in skeletal physiology and pathophysiologyMone Zaidi
Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, New York 10029, USA
Endocr Pract 16:874-81. 2010..To review new discoveries that revisit our current thinking on the genesis of osteoporosis using hypogonadal and thyrotoxic bone loss as examples... - Forty years of calcitonin--where are we now? A tribute to the work of Iain Macintyre, FRSMone Zaidi
Departments of Medicine and Geriatrics, Mount Sinai Bone Program, Mount Sinai School of Medicine, One Gustave Levy Place, Box 1055, New York, NY 10029, USA
Bone 30:655-63. 2002.... - Osteoclastogenesis, bone resorption, and osteoclast-based therapeuticsMone Zaidi
Department of Medicine, Geriatrics and Physiology and The Mount Sinai Bone Program, Bronx VA Geriatrics Research Education and Clinical Center, New York, New York, USA
J Bone Miner Res 18:599-609. 2003..The main outstanding issues, basic and translational, will be considered in relation to the osteoclast as a target for antiresorptive therapies... - TSH is a negative regulator of skeletal remodelingEtsuko Abe
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Cell 115:151-62. 2003..These studies define a role for TSH as a single molecular switch in the independent control of both bone formation and resorption... - TNFalpha mediates the skeletal effects of thyroid-stimulating hormoneHidenori Hase
Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 103:12849-54. 2006..The results suggest that TNFalpha is the critical cytokine mediating the downstream antiresorptive effects of TSH on the skeleton... - Disordered osteoclast formation and function in a CD38 (ADP-ribosyl cyclase)-deficient mouse establishes an essential role for CD38 in bone resorptionLi Sun
Mount Sinai Bone Program and Department of Medicine and Geriatrics, Mount Sinai School of Medicine, and Division of Endocrinology and Geriatric Research Education and Clinical Center GRECC, Veterans Affairs Medical Center, New York, New York 10029, USA
FASEB J 17:369-75. 2003..These findings establish a critical role for CD38 in osteoclast formation and bone resorption. We speculate that CD38 functions as a cellular NAD+ "sensor," particularly during periods of active motility and secretion... - FSH directly regulates bone massLi Sun
Mount Sinai Bone Program, Department of Medicine and Department of Orthopedics, Mount Sinai School of Medicine, New York, NY 10029, USA
Cell 125:247-60. 2006..Osteoclasts and their precursors possess G(i2alpha)-coupled FSHRs that activate MEK/Erk, NF-kappaB, and Akt to result in enhanced osteoclast formation and function. We suggest that high circulating FSH causes hypogonadal bone loss... - Calcineurin regulates bone formation by the osteoblastLi Sun
Bone Program and Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 102:17130-5. 2005..Together, the gain- and loss-of-function experiments indicate that calcineurin regulates bone formation through an effect on osteoblast differentiation... - TSH and bone lossLi Sun
Department of Medicine, Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA
Ann N Y Acad Sci 1068:309-18. 2006..The evidence that low TSH levels predispose to osteoporosis in hyperthyroidism is discussed in view of the emerging role of pituitary hormones in bone biology... - Loss of MMP-2 disrupts skeletal and craniofacial development and results in decreased bone mineralization, joint erosion and defects in osteoblast and osteoclast growthRebecca A Mosig
Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA
Hum Mol Genet 16:1113-23. 2007..Thus, Mmp2-/- mice provide a valuable biological resource for studying the pathophysiological mechanisms underlying the human disease and defining the in vivo physiological role of MMP-2... - Intermittent recombinant TSH injections prevent ovariectomy-induced bone lossLi Sun
The Mount Sinai Bone Program and The Thyroid Research Unit at the Bronx Veterans Affairs Medical Center, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 105:4289-94. 2008..In contrast, loss of function of a mutant TSHR (Pro --> Leu at 556) in congenital hypothyroid mice activates osteoclast differentiation, confirming once again our premise that TSHRs have a critical role in regulating bone remodeling... - Impaired osteoblastic differentiation, reduced bone formation, and severe osteoporosis in noggin-overexpressing miceXue Bin Wu
Division of Endocrinology, Diabetes, and Bone Diseases, Mount Sinai School of Medicine, One Gustave L Levy Place, Box 1055, New York, New York 10029, USA
J Clin Invest 112:924-34. 2003..Thus, the overproduction of noggin during biological aging may result in impaired osteoblast formation and function and hence, net bone loss... - Cellular and molecular consequences of calcineurin A alpha gene deletionLi Sun
Mount Sinai Bone Program and Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Ann N Y Acad Sci 1116:216-26. 2007..We speculate that the so-called "calcineurin inhibitors" may interact with molecules other than calcineurin. The clinical relevance of these observations is explored... - Adenosine A(1) receptors regulate bone resorption in mice: adenosine A(1) receptor blockade or deletion increases bone density and prevents ovariectomy-induced bone loss in adenosine A(1) receptor-knockout miceFiras M Kara
New York University School of Medicine, New York, NY, USA
Arthritis Rheum 62:534-41. 2010.... - Bone loss in thyroid disease: role of low TSH and high thyroid hormoneEtsuko Abe
Mount Sinai Bone Program and The Thyroid Research Unit at the James Peter s Veterans Affairs Medical Center, Mount Sinai School of Medicine, New York, NY 10029, USA
Ann N Y Acad Sci 1116:383-91. 2007..We can now provide results that not thyroid hormones but also TSH itself has an equally important role to play in bone remodeling... - A novel mechanism for coupling cellular intermediary metabolism to cytosolic Ca2+ signaling via CD38/ADP-ribosyl cyclase, a putative intracellular NAD+ sensorLi Sun
Mount Sinai Bone Program, Department of Medicine, and Bronx Veterans Affairs Geriatrics Research Education and Clinical Center (GRECC, New York, New York 10029, USA
FASEB J 16:302-14. 2002..Finally, ryanodine inhibited Ca2+ signaling, indicating the downstream activation of ryanodine receptors by cADPr. We conclude that intracellularly expressed CD38 might link cellular NAD+ production to cytosolic Ca2+ signaling... - Physiological loading of joints prevents cartilage degradation through CITED2Daniel J Leong
Leni and Peter W May Department of Orthopedics, Mount Sinai School of Medicine, One Gustave L Levy Pl, New York, NY 10029, USA
FASEB J 25:182-91. 2011..Together, these studies identify a novel regulatory pathway involving CITED2 and p38δ, which may be critical for the maintenance of articular cartilage integrity under normal physical activity levels... - The thyroid-stimulating hormone receptor: impact of thyroid-stimulating hormone and thyroid-stimulating hormone receptor antibodies on multimerization, cleavage, and signalingRauf Latif
Thyroid Research Unit, Mount Sinai School of Medicine and the James J Peters VA Medical Center, New York, NY 10468, USA
Endocrinol Metab Clin North Am 38:319-41, viii. 2009..Knowledge of the structure/function relationship of the TSHR is beginning to provide a greater understanding of thyroid physiology and thyroid autoimmunity... - Molecular cloning, expression, and function of osteoclastic calcineurin AalphaLi Sun
Mount Sinai Bone Program and Division of Endocrinology, Mount Sinai School of Medicine, New York, 10029, USA
Am J Physiol Renal Physiol 284:F575-83. 2003.... - Molecular regulation of mechanotransductionJameel Iqbal
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Biochem Biophys Res Commun 328:751-5. 2005.... - Calcitonin and bone formation: a knockout full of surprisesMone Zaidi
Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, New York, USA
J Clin Invest 110:1769-71. 2002 - Further evidence for direct pro-resorptive actions of FSHLi Sun
Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA
Biochem Biophys Res Commun 394:6-11. 2010..On the basis of accumulating evidence, we reaffirm that FSH contributes to the rapid peri-menopausal and early post-menopausal bone loss, which might thus be amenable to FSH blockade... - Follicle-stimulating hormone stimulates TNF production from immune cells to enhance osteoblast and osteoclast formationJameel Iqbal
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 103:14925-30. 2006..Ascorbic acid may prevent FSH-induced hypogonadal bone loss by modulating the catabolic actions of TNFalpha... - Evidence that calcineurin is required for the genesis of bone-resorbing osteoclastsLi Sun
Mount Sinai Bone Program and Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Am J Physiol Renal Physiol 292:F285-91. 2007..Together, the gain- and loss-of-function experiments establish that calcineurin Aalpha is necessary for osteoclast formation from its precursor and that this occurs via an NFATc1-dependent mechanism... - Nandrolone slows hindlimb bone loss in a rat model of bone loss due to denervationChristopher P Cardozo
James J Peters VA Medical Center, Bronx, NY, USA
Ann N Y Acad Sci 1192:303-6. 2010..This study offers a potential novel pharmacological strategy for use of nandrolone to reduce bone loss in severe disuse- and denervation-related bone loss, such as that which occurs after spinal cord injury... - Commentary-FSH and bone 2010: evolving evidenceJameel Iqbal
The Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, New York, USA
Eur J Endocrinol 163:173-6. 2010..strengthen the view for a primary role of FSH signaling in the regulation of bone mass and bone remodeling in humans by demonstrating that an 'activating' polymorphism AA rs6166 causes low bone mass and high bone turnover... - Calcium sensing and cell signaling processes in the local regulation of osteoclastic bone resorptionMone Zaidi
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Biol Rev Camb Philos Soc 79:79-100. 2004.... - Progression of efficacy with ibandronate: a paradigm for the development of new bisphosphonatesMone Zaidi
The Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA
Ann N Y Acad Sci 1117:273-82. 2007..The ibandronate story should serve as an important future paradigm for bisphosphonate development... - Role of the pituitary-bone axis in skeletal pathophysiologyAliza Imam
The Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, New York, USA
Curr Opin Endocrinol Diabetes Obes 16:423-9. 2009..We propose a paradigm shift in endocrine physiology, which is that these hormones act by design on bone directly, also now considered an endocrine organ... - Oxytocin deficiency impairs maternal skeletal remodelingXuan Liu
Mount Sinai School of Medicine, NY, USA
Biochem Biophys Res Commun 388:161-6. 2009..We suggest that OT facilitates intergenerational transfer of calcium ions from a pregnant mother to the pups... - Structure and functional regulation of the CD38 promoterLi Sun
Mount Sinai Bone Program and Department of Medicine, Mount Sinai School of Medicine, NY, USA
Biochem Biophys Res Commun 341:804-9. 2006.... - Prostaglandin E2 modulates components of the Wnt signaling system in bone and prostate cancer cellsXin Hua Liu
Department of Medicine, Division of Endocrinology and Metabolism, Mount Sinai School of Medicine, New York, NY 10029, USA
Biochem Biophys Res Commun 394:715-20. 2010..These data demonstrate that there are dose-dependent effects of PGE(2) on Wnt activation in osteoblast-lineage cells and Wnt-inhibitor expression in PCa cells which may have clinical implications in the management... - Osteoporosis: trends and interventionAngela M Inzerillo
Mount Sinai Bone Program, Department of Medicine, Division of Endocrinology, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA
Mt Sinai J Med 69:220-31. 2002..Various therapeutic approaches now in use, and some promising experimental trials, will be discussed... - Ca(2+) influx through the osteoclastic plasma membrane ryanodine receptorBaljit S Moonga
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, Bronx Veterans Affairs Medical Center, New York 10029, USA
Am J Physiol Renal Physiol 282:F921-32. 2002..It is likely therefore that the surface RyR-2 not only gates Ca(2+) influx but also functions as a sensor for extracellular divalent cations... - Selective upregulation of the ADP-ribosyl cyclases CD38 and CD157 by TNF but not by RANK-L reveals differences in downstream signalingJameel Iqbal
Department of Endocrinology, Mount Sinai School of Medicine, New York, NY 10029, USA
Am J Physiol Renal Physiol 291:F557-66. 2006.... - Bisphosphonates induce inflammation and rupture of atherosclerotic plaques in apolipoprotein-E null miceMona Shimshi
Department of Medicine, The Mount Sinai Bone Program, The Zena and Michael A Wiener Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY 07936 1080, USA
Biochem Biophys Res Commun 328:790-3. 2005..Our finding of plaque inflammation and rupture in bisphosphonate-treated Apo-E-/- mice may provide the first animal model for studies aimed at characterizing mechanisms of plaque rupture in animal models... - Disorders associated with acute rapid and severe bone lossSolomon Epstein
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
J Bone Miner Res 18:2083-94. 2003..However, more severe forms of bone loss that result from an osteoblastic defect and reduced bone formation may benefit potentially more from newer anabolic agents, such as recombinant human parathyroid hormone (rhPTH)... - Calcitonin: physiological actions and clinical applicationsAngela M Inzerillo
Mount Sinai Bone Program, Departments of Medicine and Geriatrics, Mount Sinai School of Medicine, and Bronx Veteran's Affairs, New York, NY, USA
J Pediatr Endocrinol Metab 17:931-40. 2004.... - Proresorptive actions of FSH and bone lossMone Zaidi
Mount Sinai Bone Program, The Mount Sinai School of Medicine, New York, NY 10029, USA
Ann N Y Acad Sci 1116:376-82. 2007..Potential therapeutic implications include the development of antagonists to both circulating FSH and its osteoclastic receptor... - Regulation of FSH receptor promoter activation in the osteoclastSamir Zaidi
Mount Sinai Bone Program, Mount Sinai School of Medicine, One Gustave L Levy Place, NY 10029, USA
Biochem Biophys Res Commun 361:910-5. 2007..We surmise that the FSHR expression is regulated distinctly in the osteoclast, and differently from other cells, such as the ovarian follicular and Leydig cells... - Induction of a program gene expression during osteoblast differentiation with strontium ranelateLing Ling Zhu
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Biochem Biophys Res Commun 355:307-11. 2007..The increased osteoblastic differentiation is the likely basis underlying the therapeutic bone-forming actions of strontium ranelate... - CD38 is required for priming by TNF-alpha: a mechanism for extracellular coordination of cell fateJameel Iqbal
Mount Sinai Bone Program, Mount Sinai School of Medicine, Box 1055, 1 Gustave Levy Place, New York, NY 10029, USA
Am J Physiol Renal Physiol 292:F1283-90. 2007..Since CD38 is an ectoenzyme, we suggest that the modulation of extracellular NAD(+) metabolism likely serves as a unique mechanism to coordinate the fate of cells within a local environment... - Extracellular NAD+ metabolism modulates osteoclastogenesisJameel Iqbal
Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA
Biochem Biophys Res Commun 349:533-9. 2006..As CD38 is the major NAD+ -degrading enzyme present in the bone marrow, these results suggest that CD38-mediated inhibition of osteoclastogenesis is related to its NADase activity, not its ADPribosyl cyclase activity... - The second conference on skeletal medicine and biology: special featuresMone Zaidi
Mount Sinai Bone Program and Department of Medicine, Mount Sinai School of Medicine, New York NY 10029, USA
Ann N Y Acad Sci 1117:xiii-xix. 2007 - Modeling of serum C-telopeptide levels with daily and monthly oral ibandronate in humansMone Zaidi
Mount Sinai School of Medicine, One Gustave L Levy Place, Box 1055, New York, NY 10029, USA
Ann N Y Acad Sci 1068:560-3. 2006.... - Skeletal morphofunctional considerations and the pituitary-thyroid axisJameel Iqbal
Mount Sinai Bone Program and Department of Medicine, Mount Sinai School of Medicine, New York 10029, USA
Front Biosci (Schol Ed) 1:92-107. 2009..The current review describes these molecular mechanisms in relation to the way thyroid hormones, and the pituitary hormone thyrotropin (TSH), regulate skeletal morphogenesis and remodeling... - Restoration of bone mass in hpg mouse by preoptic area graftingGopalan Rajendren
Department of Medicine, The Mount Sinai Bone Program, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA
Ann N Y Acad Sci 1068:341-7. 2006..This establishes that the low bone mass that occurs in old hpg mice can be fully and rapidly ameliorated by preoptic area grafting... - Functional grouping of osteoclast genes revealed through microarray analysisGuozhe Yang
Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029, USA
Biochem Biophys Res Commun 366:352-9. 2008..We discuss herein the relevance of these functional gene clusters and their modulation to biological processes underlying the formation, function, and fate of osteoclasts... - Neural surveillance of skeletal homeostasisMone Zaidi
Department of Medicine and The Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, New York 10029, USA
Cell Metab 1:219-21. 2005..2005)... - The crossover of bisphosphonates to cancer therapyMerry Sun
The Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA
Ann N Y Acad Sci 1211:107-12. 2010..This review explores bisphosphonates' current clinical utility and potential as a crossover cancer therapy... - Calcitonin: the other thyroid hormoneAngela M Inzerillo
Mount Sinai Bone Program, Department of Medicine, Mount Sinai School of Medicine, and Bronx Veteran's Affairs Geriatric Research Education and Clinical Center (GRECC, New York, New York 10029, USA
Thyroid 12:791-8. 2002..This review surveys the cellular and molecular basis of these physiologic and clinical actions... - Identification of CITED2 as a negative regulator of fracture healingJonathan Y Lee
Leni and Peter W May Department of Orthopaedics, Mount Sinai School of Medicine, NY, USA
Biochem Biophys Res Commun 387:641-5. 2009..Taken together, the studies suggest that CITED2 is a critical upstream regulator of fracture healing. The suppression of CITED2 early after fracture may allow an optimal initiation of the healing response... - Cinacalcet hydrochloride (Amgen)Jameel Iqbal
Mount Sinai Bone Program, Division of Endocrinology, Mount Sinai School of Medicine, New York, NY 10029, USA
IDrugs 6:587-92. 2003..Cinacalcet hydrochloride was developed in an effort to improve on the poor pharmacokinetics and metabolism of tecalcet hydrochloride... - TNF-induced MAP kinase activation oscillates in timeJameel Iqbal
Department of Medicine, Mount Sinai School of Medicine, One Gustave L Levy Place, P O Box 1055, New York, NY 10029, USA
Biochem Biophys Res Commun 371:906-11. 2008..In view of the discovery that multiple phosphorylation pathways display dynamic oscillations, time-resolved, instead of static, measurements of kinase phosphorylation should become the experimental norm... - Low TSH triggers bone loss: fact or fiction?Mone Zaidi
Thyroid 16:1075-6. 2006 - Osteoclast signalling pathwaysHarry C Blair
Department of Pathology, University of Pittsburgh, Veterans Affairs Health System, Pittsburgh, PA 15261, USA
Biochem Biophys Res Commun 328:728-38. 2005.... - Osteoclastic differentiation and function regulated by old and new pathwaysHarry C Blair
Department of Pathology, University of Pittsburgh and Veterans Affairs Health System, Pittsburgh, PA 15261, USA
Rev Endocr Metab Disord 7:23-32. 2006..Recent findings suggest that there is a network of cytoplasmic adapters, including Gab-2 and BCAR1, which are modified by multiple signalling mechanisms and which serve to integrate the signalling pathways... - Mechanisms balancing skeletal matrix synthesis and degradationHarry C Blair
Department of Pathology, University of Pittsburgh and Veteran s Affairs Health System, Pittsburgh, Pennsylvania, USA
Biochem J 364:329-41. 2002..Secondary modulation of mineral secretion and bone degradation are mediated by humoral signals, including parathyroid hormone and vitamin D, as well as the cytokines that also regulate the underlying cell differentiation... - The second conference on skeletal medicine and biology: overview and some commentsMone Zaidi
Ann N Y Acad Sci 1116:xi-xiii. 2007 - NO-dependent osteoclast motility: reliance on cGMP-dependent protein kinase I and VASPBeatrice B Yaroslavskiy
Department of Pathology, University of Pittsburgh and Veteran's Affairs Medical Center, Pittsburgh, PA 15243, USA
J Cell Sci 118:5479-87. 2005..VASP knockdown also altered distribution of alphavbeta3 at the attachment site. We conclude that PKG I and VASP are essential for reorganization of attachment and cytoplasmic proteins in motility induced by NO or by cGMP... - Efficacy and tolerability of intravenous ibandronate injections in postmenopausal osteoporosis: 2-year results from the DIVA studyJohn A Eisman
Garvan Institute of Medical Research, St Vincent s Campus and University of New South Wales, Sydney, Australia
J Rheumatol 35:488-97. 2008..We report the effects on lumbar spine and proximal femur bone mineral density (BMD) and bone resorption markers over 2 years... - Molecules, mechanisms, and momentum in bone and cartilage researchMone Zaidi
Biochem Biophys Res Commun 328:647-50. 2005 - Mitochondria to nucleus stress signaling: a distinctive mechanism of NFkappaB/Rel activation through calcineurin-mediated inactivation of IkappaBbetaGopa Biswas
Dept of Animal Biology, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
J Cell Biol 161:507-19. 2003..The results provide new insights into the role of Cn as a critical link between Ca2+ signaling and NFkappaB/Rel activation... - Similarities and contrasts in ryanodine receptor localization and function in osteoclasts and striated muscle cellsChristopher L H Huang
Physiological Laboratory, University of Cambridge, Cambridge, UK
Ann N Y Acad Sci 1116:255-70. 2007..Such a mechanism could interact with other osteoclast processes transferring Ca(2+) between cytosol, intracellular stores and extracellular space and be integrated with systemic processes regulating Ca(2+) homeostasis...
Research Grants
- TSH and BoneMone Zaidi; Fiscal Year: 2009..This proposal examines the molecular mechanism through which TSH acts directly on the skeleton. ..
- Role of FSH in Osreoclast Formation and FunctionMone Zaidi; Fiscal Year: 2010....
- The Role of NFATc1 and Calcineurin in Bone RemodelingMone Zaidi; Fiscal Year: 2007....
- Calcium in the regulation of osteoclast formationMone Zaidi; Fiscal Year: 2007..Finally, we will determine whether CD38 over-expression in transgenic mice results in an osteopetrotic phenotype and dysfunctional osteoclasts...
- Skeletal Biology and Medicine ConferenceMone Zaidi; Fiscal Year: 2007....
- Calcium in the regulation of osteoclast formationMone Zaidi; Fiscal Year: 2007..abstract_text> ..
- TSH and BoneMONE contact ZAIDI; Fiscal Year: 2010..This proposal examines the molecular mechanism through which TSH acts directly on the skeleton. ..
- Role of FSH in Osreoclast Formation and FunctionMone Zaidi; Fiscal Year: 2009....
- CD38/ADP RIBOSYL CYCLASE R0LE IN OSTEOCLAST REGULATIONMone Zaidi; Fiscal Year: 2003..Taken together, the studies should provide mechanistic insights into the role of the NAD+/CD38/cADPr/Ca2+ system in osteoclast control. ..
- Skeletal Development and Remodeling in Health, Disease and AgingMone Zaidi; Fiscal Year: 2005..A local forum, which will provide the non-scientific public an informal opportunity to learn about the latest research and therapies emerging in the field, is also planned. ..
- TSH and BoneMONE contact ZAIDI; Fiscal Year: 2010..We showed that decrements in the pituitary hormone TSH accompany the high thyroid hormone levels, both of which contribute to the bone loss. This proposal examines the molecular mechanism through which TSH acts directly on the skeleton. ..