Wilma and Roswell Messing Professor, Pathology and Immunology, Washington University School of Medicine
Pathology
Dr. Steven L. Teitelbaum, MD
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Steven Teitelbaum is an expert in the field of Pathology. He attended NYU School of Medicine. He has 4 awards "Pieter Gaillard Founders Award", "Peter H. Raven Lifetime Achievement Award", "Carl and Gerty Cori Faculty Achievement Award" and "Elected Member". Steven Teitelbaum is a published MD. He has 72 publications published. The most current publication "ASXL2 Regulates Glucose, Lipid, and Skeletal Homeostasis."
Publications
- Correlating RANK Ligand/RANK Binding Kinetics With Osteoclast Formation and Function.
- ASXL2 Regulates Glucose, Lipid, and Skeletal Homeostasis.
- Absence of Dap12 and the αvβ3 integrin causes severe osteopetrosis.
- An insulin-sensitizing thiazolidinedione, which minimally activates PPAR?, does not cause bone loss.
- Depression, Antidepressants, and Bone Health in Older Adults: A Systematic Review.
- Vinculin Regulates Osteoclast Function.
- Genetic variation in the serotonin transporter and HTR1B receptor predicts reduced bone formation during serotonin reuptake inhibitor treatment in older adults.
- Zap70 inhibits Syk-mediated osteoclast function.
- Serotonin-norepinephrine reuptake inhibitor therapy in late-life depression is associated with increased marker of bone resorption.
- Type I Phosphotidylinosotol-4 Phosphate 5 Kinase ? Regulates Osteoclasts in a Bifunctional Manner.
- The osteoclast and its unique cytoskeleton.
- Autophagy proteins regulate the secretory component of osteoclastic bone resorption.
- Oophorectomy-induced bone loss is attenuated in MAGP1-deficient mice.
- Mouse genome-wide association and systems genetics identify asxl2 as a regulator of bone mineral density and osteoclastogenesis.
- Calpain-6, a target molecule of glucocorticoids, regulates osteoclastic bone resorption via cytoskeletal organization and microtubule acetylation.
- Should bisphosphonates be used for long-term treatment of glucocorticoid-induced osteoporosis?
- Fyn promotes proliferation, differentiation, survival and function of osteoclast lineage cells.
- Stem cells and osteoporosis therapy.
- Microfibril-associated glycoprotein-1, an extracellular matrix regulator of bone remodeling.
- Osteoclast-specific inactivation of the integrin-linked kinase (ILK) inhibits bone resorption.
- Cdc42 regulates bone modeling and remodeling in mice by modulating RANKL/M-CSF signaling and osteoclast polarization.
- Src-like adaptor protein regulates osteoclast generation and survival.
- Dissection of platelet and myeloid cell defects by conditional targeting of the beta3-integrin subunit.
- Integrins, growth factors, and the osteoclast cytoskeleton.
- How do bone cells secrete proteins?
- Defects in osteoblast function but no changes in long-term repopulating potential of hematopoietic stem cells in a mouse chronic inflammatory arthritis model.
- SLP-76 couples Syk to the osteoclast cytoskeleton.
- Syk tyrosine 317 negatively regulates osteoclast function via the ubiquitin-protein isopeptide ligase activity of Cbl.
- Osteoclasts and arthritis.
- The Src family kinase, Lyn, suppresses osteoclastogenesis in vitro and in vivo.
- Tumor necrosis factor receptor-associated factor 6 is an intranuclear transcriptional coactivator in osteoclasts.
- DAP12 couples c-Fms activation to the osteoclast cytoskeleton by recruitment of Syk.
- Synaptotagmin VII regulates bone remodeling by modulating osteoclast and osteoblast secretion.
- NOTCH1 regulates osteoclastogenesis directly in osteoclast precursors and indirectly via osteoblast lineage cells.
- Notch signaling maintains bone marrow mesenchymal progenitors by suppressing osteoblast differentiation.
- The osteoclast: friend or foe?
- Glucocorticoids and the osteoclast.
- Bone weighs in on obesity.
- c-Fms tyrosine 559 is a major mediator of M-CSF-induced proliferation of primary macrophages.
- M-CSF regulates the cytoskeleton via recruitment of a multimeric signaling complex to c-Fms Tyr-559/697/721.
- Syk, c-Src, the alphavbeta3 integrin, and ITAM immunoreceptors, in concert, regulate osteoclastic bone resorption.
- Osteoclasts: what do they do and how do they do it?
- Noninvasive imaging of osteoclasts in parathyroid hormone-induced osteolysis using a 64Cu-labeled RGD peptide.
- The LIM protein, Limd1, regulates AP-1 activation through an interaction with Traf6 to influence osteoclast development.
- Dexamethsone suppresses bone formation via the osteoclast.
- SHIP1 negatively regulates proliferation of osteoclast precursors via Akt-dependent alterations in D-type cyclins and p27.
- Glucocorticoids suppress bone formation via the osteoclast.
- Osteoclasts and integrins.
- Critical role of beta3 integrin in experimental postmenopausal osteoporosis.
- M-CSF mediates TNF-induced inflammatory osteolysis.
- FHL2 inhibits the activated osteoclast in a TRAF6-dependent manner.
- Rab3D regulates a novel vesicular trafficking pathway that is required for osteoclastic bone resorption.
- Osteoporosis and integrins.
- Unoccupied alpha(v)beta3 integrin regulates osteoclast apoptosis by transmitting a positive death signal.
- Vav3 regulates osteoclast function and bone mass.
- IL-1 mediates TNF-induced osteoclastogenesis.
- Mice lacking the integrin beta5 subunit have accelerated osteoclast maturation and increased activity in the estrogen-deficient state.
- Postmenopausal osteoporosis, T cells, and immune dysfunction.
- Marrow stromal cells and osteoclast precursors differentially contribute to TNF-alpha-induced osteoclastogenesis in vivo.
- RANKing c-Jun in osteoclast development.
- The HIV protease inhibitor ritonavir blocks osteoclastogenesis and function by impairing RANKL-induced signaling.
- High dose M-CSF partially rescues the Dap12-/- osteoclast phenotype.
- Direct inhibition of NF-kappa B blocks bone erosion associated with inflammatory arthritis.
- The IkappaB function of NF-kappaB2 p100 controls stimulated osteoclastogenesis.
- Dynamic changes in the osteoclast cytoskeleton in response to growth factors and cell attachment are controlled by beta3 integrin.
- c-Fms and the alphavbeta3 integrin collaborate during osteoclast differentiation.
- Tyrosines 559 and 807 in the cytoplasmic tail of the macrophage colony-stimulating factor receptor play distinct roles in osteoclast differentiation and function.
- Animal rights pressure on scientists.
- SHIP-deficient mice are severely osteoporotic due to increased numbers of hyper-resorptive osteoclasts.
- Interleukin-4 reversibly inhibits osteoclastogenesis via inhibition of NF-kappa B and mitogen-activated protein kinase signaling.
- Manipulation of receptor oligomerization as a strategy to inhibit signaling by TNF superfamily members.
Schools
Washington Center School of Medicine
Barnes Jewish Hospital
Bellevue Hospital Center
Doctors Specialties
- Pathology
Accepted Insurances
Awards
- Pieter Gaillard Founders Award
- Peter H. Raven Lifetime Achievement Award
- Carl and Gerty Cori Faculty Achievement Award
- Elected Member
Education
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NYU School of Medicine -
Washington University - Barnes-Jewish Hospital -
Washington University School of Medicine in St. Louis
Hospital
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Barnes-Jewish Hospital
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