Altered endochondral bone development in matrix metalloproteinase 13-deficient mice. - Wikidata - awgldk - TriplyDB

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

http://www.wikidata.org/entity/Q37407318

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A secreted tyrosine kinase acts in the extracellular environment MMP13 mutation causes spondyloepimetaphyseal dysplasia, Missouri type (SEMD(MO)Attenuation of osteoarthritis progression by reduction of discoidin domain receptor 2 in mice Osteoarthritis pathogenesis: a review of molecular mechanisms Cartilage to bone transitions in health and disease A pathway to bone: signaling molecules and transcription factors involved in chondrocyte development and maturation The roles of hyaluronan/RHAMM/CD44 and their respective interactions along the insidious pathways of fibrosarcoma progression A human laterality disorder caused by a homozygous deleterious mutation in MMP21 Autonomous regulation of osteosarcoma cell invasiveness by Wnt5a/Ror2 signaling TGF-β signaling plays an essential role in the growth and maintenance of intervertebral disc tissue Role of matrix metalloproteinase 13 in both endochondral and intramembranous ossification during skeletal regeneration Membrane-type MMPs enable extracellular matrix permissiveness and mesenchymal cell proliferation during embryogenesis Type I collagen is a genetic modifier of matrix metalloproteinase 2 in murine skeletal development Parathyroid hormone activation of matrix metalloproteinase-13 transcription requires the histone acetyltransferase activity of p300 and PCAF and p300-dependent acetylation of PCAF MEPE is a novel regulator of growth plate cartilage mineralization Galectin-3 is a downstream regulator of matrix metalloproteinase-9 function during endochondral bone formation.The extracellular matrix: a dynamic niche in cancer progression Matrix metalloproteinases and the regulation of tissue remodelling Genes responsive to low-intensity pulsed ultrasound in MC3T3-E1 preosteoblast cells.Genome-wide isolation of growth and obesity QTL using mouse speed congenic strains.Inhibition of ALK5 signaling induces physeal dysplasia in rats.High throughput screening of potentially selective MMP-13 exosite inhibitors utilizing a triple-helical FRET substrate.Matrix metalloproteinase 13 is induced in fibroblasts in polyomavirus middle T antigen-driven mammary carcinoma without influencing tumor progression.The Wnt/beta-catenin pathway interacts differentially with PTHrP signaling to control chondrocyte hypertrophy and final maturation Identification of the GATA factor TRPS1 as a repressor of the osteocalcin promoter.Genome-wide analyses of gene expression during mouse endochondral ossification Expression of cartilage developmental genes in Hoxc8- and Hoxd4-transgenic mice.p63 transcriptionally regulates the expression of matrix metallopeptidase 13.Specific expression of Cre recombinase in hypertrophic cartilage under the control of a BAC-Col10a1 promoter.Progress in matrix metalloproteinase research.Molecular pathology of vertebral deformities in hyperthermic Atlantic salmon (Salmo salar)Matrix metalloproteinase 13-deficient mice are resistant to osteoarthritic cartilage erosion but not chondrocyte hypertrophy or osteophyte development.Tissue inhibitor of metalloproteinase-3 (TIMP-3) regulates hematopoiesis and bone formation in vivo.Temporal gene expression profiling during rat femoral marrow ablation-induced intramembranous bone regeneration Matrix metalloproteinases are not essential for aggrecan turnover during normal skeletal growth and development.Upregulation of MMP-13 and TIMP-1 expression in response to mechanical strain in MC3T3-E1 osteoblastic cells.Stromal regulation of vessel stability by MMP14 and TGFbeta.Phenotypic overlap between MMP-13 and the plasminogen activation system during wound healing in mice.Recapitulation of endochondral bone formation using human adult mesenchymal stem cells as a paradigm for developmental engineering.Complementary interplay between matrix metalloproteinase-9, vascular endothelial growth factor and osteoclast function drives endochondral bone formation

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Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

http://www.wikidata.org/entity/Q37407318

description

article científic

@ca

article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on December 2004

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

@en

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

@nl

type

label

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

@en

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

@nl

prefLabel

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

@en

Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

@nl

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Altered endochondral bone development in matrix metalloproteinase 13-deficient mice.

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Amanda J Fosang

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Babette Heyer

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Bettina Hartenstein

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Danielle J Behonick

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Dominique Stickens

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Marina Schorpp-Kistner

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Nathalie Ortega

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Peter Angel

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Ying Yu

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Zena Werb

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P2860

Purification and cloning of aggrecanase-1: a member of the ADAMTS family of proteins

Cloning and characterization of ADAMTS11, an aggrecanase from the ADAMTS family

Dominant mutations in the type II collagen gene, COL2A1, produce spondyloepimetaphyseal dysplasia, Strudwick type

MMP13 mutation causes spondyloepimetaphyseal dysplasia, Missouri type (SEMD(MO)

Cloning, expression, and type II collagenolytic activity of matrix metalloproteinase-13 from human osteoarthritic cartilage

MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes

Spondylo-epi-metaphyseal dysplasia (SEMD) matrilin 3 type: homozygote matrilin 3 mutation in a novel form of SEMD

ADAMTS-1 cleaves a cartilage proteoglycan, aggrecan

Inducible gene targeting in mice using the Cre/lox system

Cellular mechanisms for human procollagenase-3 (MMP-13) activation. Evidence that MT1-MMP (MMP-14) and gelatinase a (MMP-2) are able to generate active enzyme

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10.1242/DEV.01461

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