Increased Classical Endoplasmic Reticulum Stress Is Sufficient to Reduce Chondrocyte Proliferation Rate in the Growth Plate and Decrease Bone Growth
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Title
Increased Classical Endoplasmic Reticulum Stress Is Sufficient to Reduce Chondrocyte Proliferation Rate in the Growth Plate and Decrease Bone Growth
Authors
Keywords
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Journal
PLoS One
Volume 10, Issue 2, Pages e0117016
Publisher
Public Library of Science (PLoS)
Online
2015-02-19
DOI
10.1371/journal.pone.0117016
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- (2014) Sara E. Patterson et al. DEVELOPMENTAL DYNAMICS
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- (2013) B. Gualeni et al. Disease Models & Mechanisms
- Development of the Endochondral Skeleton
- (2013) F. Long et al. Cold Spring Harbor Perspectives in Biology
- Analysis of the cartilage proteome from three different mouse models of genetic skeletal diseases reveals common and discrete disease signatures
- (2013) P. A. Bell et al. Biology Open
- Hypertrophic Chondrocytes Have a Limited Capacity to Cope with Increases in Endoplasmic Reticulum Stress without Triggering the Unfolded Protein Response
- (2012) Louise H. W. Kung et al. JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
- Nosology and classification of genetic skeletal disorders: 2010 revision
- (2011) Matthew L. Warman et al. AMERICAN JOURNAL OF MEDICAL GENETICS PART A
- A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia
- (2011) Farhana Suleman et al. HUMAN MUTATION
- The skeleton: a multi-functional complex organ. The growth plate chondrocyte and endochondral ossification
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- ENU-induced missense mutation in the C-propeptide coding region of Col2a1 creates a mouse model of platyspondylic lethal skeletal dysplasia, Torrance type
- (2011) Tatsuya Furuichi et al. MAMMALIAN GENOME
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- An unfolded protein response is the initial cellular response to the expression of mutant matrilin-3 in a mouse model of multiple epiphyseal dysplasia
- (2010) Seema Nundlall et al. CELL STRESS & CHAPERONES
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- (2010) J. L. Goeckeler et al. DIABETES OBESITY & METABOLISM
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- (2010) Atsushi Saito et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- An Inducible Cartilage Oligomeric Matrix Protein Mouse Model Recapitulates Human Pseudoachondroplasia Phenotype
- (2009) Karen L. Posey et al. AMERICAN JOURNAL OF PATHOLOGY
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- (2009) Raymond P. Boot-Handford et al. CELL AND TISSUE RESEARCH
- Regulation of endoplasmic reticulum stress response by a BBF2H7-mediated Sec23a pathway is essential for chondrogenesis
- (2009) Atsushi Saito et al. NATURE CELL BIOLOGY
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- Thrombospondins: from structure to therapeutics
- (2008) K. L. Posey et al. CELLULAR AND MOLECULAR LIFE SCIENCES
- Endoplasmic Reticulum (ER) Chaperone Regulation and Survival of Cells Compensating for Deficiency in the ER Stress Response Kinase, PERK
- (2008) Yukihiro Yamaguchi et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- PERK is essential for neonatal skeletal development to regulate osteoblast proliferation and differentiation
- (2008) Jianwen Wei et al. JOURNAL OF CELLULAR PHYSIOLOGY
- Endochondral ossification: How cartilage is converted into bone in the developing skeleton
- (2007) E.J. Mackie et al. INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
- Transgenic mice expressing D469Δ mutated cartilage oligomeric matrix protein (COMP) show growth plate abnormalities and sternal malformations
- (2007) Markus Schmitz et al. MATRIX BIOLOGY
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