Abstracts tagged "osteoclasts and signal transduction"

Abstract Number: 2085 • 2015 ACR/ARHP Annual Meeting
DC-STAMP Regulates Osteoclastogenesis through the Ca2+ /NFATc1 Axis
Yahui Grace Chiu¹, Dongge Li², Yue-Xin Xu³, Tzong-Ren Sheu⁴, Minsoo Kim⁵ and Christopher T. Ritchlin⁶, ¹Allergy, Immunology, and Rheumatology, University of Rochester, Rochester, NY, ²Allergy, Immunology and Rheumatology, University of Rochester, Rochester, NY, ³Microbiology & Immunology, University of Rochester, Rochester, NY, ⁴Center for Musculoskeletal Research, University of Rochester, Rochester, NY, ⁵Microbiology and Immunology, University of Rochester, Rochester, NY, ⁶Allergy, Immunology and Rheumatololgy Division, University of Rochester Medical Center, Rochester, NY
Background/Purpose: Osteoclasts (OC) are the only cell type known to erode bone. Many bone diseases including osteoporosis and arthritis are caused by excessive OC activity.…
Abstract Number: 2794 • 2014 ACR/ARHP Annual Meeting
Deletion of the Inhibitory Receptor Motif, ITIM, on DC-STAMP Alters Osteoclast Differentiation and Function
Yahui Grace Chiu¹, Edward M. Schwarz², Dongge Li¹, Yuexin Xu³, Minsoo Kim³ and Christopher T. Ritchlin⁴, ¹Allergy, Immunology and Rheumatology, University of Rochester, Rochester, NY, ²Center for Musculoskeletal Research, University of Rochester, Rochester, NY, ³Microbiology and Immunology, University of Rochester, Rochester, NY, ⁴Allergy Immunology & Rheumatology, University of Rochester Medical Center, Rochester, NY
Background/Purpose DC-STAMP (Dendritic Cell-Specific Transmembrane Protein), a 7-pass transmembrane protein essential for cell-to-cell fusion during osteoclast (OC) differentiation, is expressed on the cell surface of…
Abstract Number: 23 • 2014 ACR/ARHP Annual Meeting
Activation of EPAC1/2 Is Essential for Osteoclast Formation By Modulating NFkB Nuclear Translocation and Actin Cytoskeleton Rearrangements
Aranzazu Mediero¹, Miguel Perez-Aso² and Bruce N. Cronstein³, ¹Medicine, Division of Translational Medicine, NYU School of Medicine, New York, NY, ²545 1st Ave., New York University, New York City, NY, ³NYU School of Medicine, Division of Rheumatology, New York, NY
Background/Purpose Bisphosphonates inhibit osteoclast differentiation/function via inhibition of Rap1A isoprenylation and cytoskeletal assembly. As Rap1 is the effector of EPAC proteins (exchange protein directly activated…
Abstract Number: 1799 • 2012 ACR/ARHP Annual Meeting
ONO-4059 – A Novel Small Molecule Bruton’s Tyrosine Kinase (Btk) Inhibitor, Suppresses Osteoclast Differentiation and Activation
Yuko Ariza, Toshio Yoshizawa, Yoshiko Ueda, Shingo Hotta, Masami Narita and Kazuhito Kawabata, Discovery Research Laboratories 3, Ono Pharmaceutical Co., Ltd., Osaka, Japan
Background/Purpose: Bruton’s tyrosine kinase (Btk) is primarily expressed in B cells, mast cells, platelets, myeloid cells and osteoclasts. Osteoclast differentiation is regulated by signaling pathways…
Abstract Number: 14 • 2012 ACR/ARHP Annual Meeting
EPAC1 Activation Is Required for NFkB Nuclear Translocation and Osteoclast Differentiation
Aranzazu Mediero¹ and Bruce N. Cronstein², ¹Medicine, Division of Translational Medicine, NYU School of Medicine, New York, NY, ²Internal Medicine, NYU School of Medicine, Division of Rheumatology, New York, NY
Background/Purpose: Previous work demonstrated that one mechanism by which bisphosphonates inhibit osteoclast differentiation and function is via inhibition of Rap1A isoprenylation and, as a result,…
Abstract Number: 15 • 2012 ACR/ARHP Annual Meeting
Adenosine A_2A Receptor Stimulation Inhibits OC Formation by Suppressing NFkB Translocation to the Nucleus by A PKA-ERK1/2 Mediated Mechanism
Aranzazu Mediero¹ and Bruce N. Cronstein², ¹Medicine, Division of Translational Medicine, NYU School of Medicine, New York, NY, ²Internal Medicine, NYU School of Medicine, Division of Rheumatology, New York, NY
Background/Purpose: Adenosine, a nucleoside released at sites of injury and hypoxia, mediates its effects via activation of G-protein-coupled receptors (A1, A2A, A2B, A3). Previously we…

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