SHP2 Regulates Chondrocyte Terminal Differentiation, Growth Plate Architecture and Skeletal Cell Fates
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Title
SHP2 Regulates Chondrocyte Terminal Differentiation, Growth Plate Architecture and Skeletal Cell Fates
Authors
Keywords
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Journal
PLoS Genetics
Volume 10, Issue 5, Pages e1004364
Publisher
Public Library of Science (PLoS)
Online
2014-05-30
DOI
10.1371/journal.pgen.1004364
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Note: Only part of the references are listed.- Expression of collagen type I, II, X and Ki-67 in osteochondroma compared to human growth plate cartilage
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- (2013) P. E. Lapinski et al. Disease Models & Mechanisms
- An RNA-seq protocol to identify mRNA expression changes in mouse diaphyseal bone: Applications in mice with bone property alteringLrp5mutations
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- Targeted Disruption ofShp2in Chondrocytes Leads to Metachondromatosis With Multiple Cartilaginous Protrusions
- (2013) Harry KW Kim et al. JOURNAL OF BONE AND MINERAL RESEARCH
- Ptpn11 deletion in a novel progenitor causes metachondromatosis by inducing hedgehog signalling
- (2013) Wentian Yang et al. NATURE
- Induction of SHP2 Deficiency in Chondrocytes Causes Severe Scoliosis and Kyphosis in Mice
- (2013) Harry K. W. Kim et al. SPINE
- Regulation of endochondral ossification by transcription factors
- (2012) Riko Nishimura Frontiers in Bioscience-Landmark
- Primary cilia attenuate hedgehog signalling in neoplastic chondrocytes
- (2012) L Ho et al. ONCOGENE
- Can MR imaging challenge the commonly accepted theory of the pathogenesis of solitary enchondroma of long bone?
- (2012) H. Douis et al. SKELETAL RADIOLOGY
- IDH1 and IDH2 mutations are frequent events in central chondrosarcoma and central and periosteal chondromas but not in other mesenchymal tumours
- (2011) M Fernanda Amary et al. JOURNAL OF PATHOLOGY
- Ollier disease and Maffucci syndrome are caused by somatic mosaic mutations of IDH1 and IDH2
- (2011) M Fernanda Amary et al. NATURE GENETICS
- Somatic mosaic IDH1 and IDH2 mutations are associated with enchondroma and spindle cell hemangioma in Ollier disease and Maffucci syndrome
- (2011) Twinkal C Pansuriya et al. NATURE GENETICS
- Peripheral chondrosarcoma progression is associated with increased type X collagen and vascularisation
- (2011) Carlos E. de Andrea et al. VIRCHOWS ARCHIV
- Loss-of-Function Mutations in PTPN11 Cause Metachondromatosis, but Not Ollier Disease or Maffucci Syndrome
- (2011) Margot E. Bowen et al. PLoS Genetics
- From RNA-seq reads to differential expression results
- (2011) Alicia Oshlack et al. GENOME BIOLOGY
- SOX9 is a major negative regulator of cartilage vascularization, bone marrow formation and endochondral ossification
- (2010) T. Hattori et al. DEVELOPMENT
- Development of severe skeletal defects in induced SHP-2-deficient adult mice: a model of skeletal malformation in humans with SHP-2 mutations
- (2010) T. J. Bauler et al. Disease Models & Mechanisms
- Phosphate-induced Apoptosis of Hypertrophic Chondrocytes Is Associated with a Decrease in Mitochondrial Membrane Potential and Is Dependent upon Erk1/2 Phosphorylation
- (2010) Susanne U. Miedlich et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Genetic inactivation of ERK1 and ERK2 in chondrocytes promotes bone growth and enlarges the spinal canal
- (2010) Arjun Sebastian et al. JOURNAL OF ORTHOPAEDIC RESEARCH
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- (2010) T. Inoue et al. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
- Identification of light and dark hypertrophic chondrocytes in mouse and rat chondrocyte pellet cultures
- (2010) K.-S. Chen et al. TISSUE & CELL
- Whole-Genome Sequencing of a Single Proband Together with Linkage Analysis Identifies a Mendelian Disease Gene
- (2010) Nara L. M. Sobreira et al. PLoS Genetics
- Benign Cartilaginous Tumors of Bone
- (2009) Salvatore Romeo et al. ADVANCES IN ANATOMIC PATHOLOGY
- TopHat: discovering splice junctions with RNA-Seq
- (2009) Cole Trapnell et al. BIOINFORMATICS
- edgeR: a Bioconductor package for differential expression analysis of digital gene expression data
- (2009) M. D. Robinson et al. BIOINFORMATICS
- Ubiquitous overexpression of Hey1 transcription factor leads to osteopenia and chondrocyte hypertrophy in bone
- (2009) Rishard Salie et al. BONE
- Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb)
- (2009) Ivy Jennes et al. HUMAN MUTATION
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- Extracellular Signal-Regulated Kinase 1 (ERK1) and ERK2 Play Essential Roles in Osteoblast Differentiation and in Supporting Osteoclastogenesis
- (2009) T. Matsushita et al. MOLECULAR AND CELLULAR BIOLOGY
- Pten in stromal fibroblasts suppresses mammary epithelial tumours
- (2009) Anthony J. Trimboli et al. NATURE
- A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes
- (2009) K. B. Jones et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Msx2 Stimulates Chondrocyte Maturation by Controlling Ihh Expression
- (2008) Katsuhiko Amano et al. JOURNAL OF BIOLOGICAL CHEMISTRY
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- (2008) Qiuhui Pan et al. JOURNAL OF CELLULAR PHYSIOLOGY
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- (2008) Marjolaine Gosset et al. Nature Protocols
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