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      Increased RANKL-mediated osteoclastogenesis by interleukin-1β and endoplasmic reticulum stress.

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          Abstract

          The mechanism by which IL-1β and thapsigargin (TG)-induced endoplasmic reticulum (ER) stress modulate the receptor activator of nuclear factor kappa-B ligand (RANKL)-mediated osteoclastogenesis remains elusive. Thus, we investigated the osteoclast-specific and ER signals in osteoclastogenesis of bone marrow-derived cells.

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          Author and article information

          Journal
          Joint Bone Spine
          Joint, bone, spine : revue du rhumatisme
          Elsevier BV
          1778-7254
          1297-319X
          Dec 2014
          : 81
          : 6
          Affiliations
          [1 ] Department of Internal Medicine, Medical School and Research Institute of Clinical Medicine, Chonbuk National University and Chonbuk, National University Hospital, Jeonju, Jeonbuk 561-712, South Korea.
          [2 ] Department of Pharmacy Practice, College of Pharmacy, University of Rhode Island, Kingston RI 02881, United States of America.
          [3 ] Department of Pharmacology, Chonbuk National University Medical School, Jeonju, Jeonbuk 561-712, South Korea.
          [4 ] Department of Anatomy, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, Seoul 110-799, South Korea.
          [5 ] Department of Internal Medicine, Medical School and Research Institute of Clinical Medicine, Chonbuk National University and Chonbuk, National University Hospital, Jeonju, Jeonbuk 561-712, South Korea. Electronic address: ywhim@jbnu.ac.kr.
          Article
          S1297-319X(14)00132-8
          10.1016/j.jbspin.2014.04.012
          24956991
          01f1bd34-38d0-491f-8f16-c1df78bfeffe
          History

          Thapsigargin,IL-1β,Osteoclast,4-phenylbutyric acid,Endoplasmic reticulum stress

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