A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes. - Wikidata - wikimedia - TriplyDB

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

http://www.wikidata.org/entity/Q33719846

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Heparan sulfate in skeletal development, growth, and pathology: the case of hereditary multiple exostoses Hereditary Multiple Exostoses: a review of clinical appearance and metabolic pattern Secondary peripheral chondrosarcoma evolving from osteochondroma as a result of outgrowth of cells with functional EXT Loss-of-function mutations in PTPN11 cause metachondromatosis, but not Ollier disease or Maffucci syndrome.Unsuspected osteochondroma-like outgrowths in the cranial base of Hereditary Multiple Exostoses patients and modeling and treatment with a BMP antagonist in mice.EXTra hit for mouse osteochondroma.Bone Size and Quality Regulation: Concerted Actions of mTOR in Mesenchymal Stromal Cells and Osteoclasts Breakpoint characterization of large deletions in EXT1 or EXT2 in 10 multiple osteochondromas families HSPG-deficient zebrafish uncovers dental aspect of multiple osteochondromas.No haploinsufficiency but loss of heterozygosity for EXT in multiple osteochondromas Chondrosarcoma: with updates on molecular genetics.Glycobiology and the growth plate: current concepts in multiple hereditary exostoses Heparan sulfate proteoglycans.Primary neoplasms of bones in mice: retrospective study and review of literature SHP2 regulates chondrocyte terminal differentiation, growth plate architecture and skeletal cell fates FGFR3 Deficiency Causes Multiple Chondroma-like Lesions by Upregulating Hedgehog Signaling.Heparanase stimulates chondrogenesis and is up-regulated in human ectopic cartilage: a mechanism possibly involved in hereditary multiple exostoses.Rearrangement of chromosome bands 12q14~15 causing HMGA2-SOX5 gene fusion and HMGA2 expression in extraskeletal osteochondroma Genetic mouse models for bone studies--strengths and limitations The glomerular basement membrane as a model system to study the bioactivity of heparan sulfate glycosaminoglycans.Cell cycle deregulation and mosaic loss of Ext1 drive peripheral chondrosarcomagenesis in the mouse and reveal an intrinsic cilia deficiency Somatic mosaic IDH1 and IDH2 mutations are associated with enchondroma and spindle cell hemangioma in Ollier disease and Maffucci syndrome Osteochondroma of the Hyoid Bone: A Previously Unrecognized Location and Review of the Literature.Mutations in the EXT1 and EXT2 genes in Spanish patients with multiple osteochondromas.Loss of β-catenin induces multifocal periosteal chondroma-like masses in mice NFAT restricts osteochondroma formation from entheseal progenitors Toward an understanding of the short bone phenotype associated with multiple osteochondromas.Perichondrium phenotype and border function are regulated by Ext1 and heparan sulfate in developing long bones: a mechanism likely deranged in Hereditary Multiple Exostoses.Inactivation of Fam20B in Joint Cartilage Leads to Chondrosarcoma and Postnatal Ossification Defects.From an orphan disease to a generalized molecular mechanism: PTPN11 loss-of-function mutations in the pathogenesis of metachondromatosis Epiphyseal growth plate and secondary peripheral chondrosarcoma: the neighbours matter.Cell biology of osteochondromas: bone morphogenic protein signalling and heparan sulphates.Hereditary Multiple Exostoses: New Insights into Pathogenesis, Clinical Complications, and Potential Treatments.Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research.Assessing the general population frequency of rare coding variants in the EXT1 and EXT2 genes previously implicated in hereditary multiple exostoses Aberrant perichondrial BMP signaling mediates multiple osteochondromagenesis in mice Immunohistochemical Localization of Bone Morphogenetic Proteins (BMPs) and their Receptors in Solitary and Multiple Human Osteochondromas Epiphyseal abnormalities, trabecular bone loss and articular chondrocyte hypertrophy develop in the long bones of postnatal Ext1-deficient mice.Compound heterozygous loss of Ext1 and Ext2 is sufficient for formation of multiple exostoses in mouse ribs and long bones.Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference.

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A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

http://www.wikidata.org/entity/Q33719846

description

2009 nî lūn-bûn

@nan

2009 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի դեկտեմբերին հրատարակված գիտական հոդված

@hy

2009年の論文

@ja

2009年論文

@yue

2009年論文

@zh-hant

2009年論文

@zh-hk

2009年論文

@zh-mo

2009年論文

@zh-tw

2009年论文

@wuu

name

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

@ast

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

@en

type

label

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

@ast

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

@en

prefLabel

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

@ast

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes.

@en

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PNAS.0910875107

P1433

Proceedings of the National Academy of Sciences of the United States of America

P1476

A mouse model of osteochondromagenesis from clonal inactivation of Ext1 in chondrocytes

@en

P2093

Andrea Vortkamp

http://www.w3.org/2001/XMLSchema#string

Baoli Yang

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Charles Searby

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Florian Grabellus

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Gail Kurriger

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Jose A Morcuende

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Kevin B Jones

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Mario R Capecchi

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Peter J Roughley

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Virginia Piombo

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P2860

Multiple osteochondromas

The putative tumor suppressors EXT1 and EXT2 form a stable complex that accumulates in the Golgi apparatus and catalyzes the synthesis of heparan sulfate

Cloning of the putative tumour suppressor gene for hereditary multiple exostoses (EXT1)

The EXT1/EXT2 tumor suppressors: catalytic activities and role in heparan sulfate biosynthesis.

Mutations in the EXT1 and EXT2 genes in hereditary multiple exostoses.

EXT-mutation analysis and loss of heterozygosity in sporadic and hereditary osteochondromas and secondary chondrosarcomas.

Mutation and cancer: statistical study of retinoblastoma

Hereditary multiple exostoses (EXT): mutational studies of familial EXT1 cases and EXT-associated malignancies

Generalized lacZ expression with the ROSA26 Cre reporter strain

Diminished levels of the putative tumor suppressor proteins EXT1 and EXT2 in exostosis chondrocytes

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2054-2059

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scholarly article

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10.1073/PNAS.0910875107

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5

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107

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Val C Sheffield

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2009-12-22T00:00:00Z

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41040259

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20080592

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Exostosin glycosyltransferase 1

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2836675

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