Targeted induction of endoplasmic reticulum stress induces cartilage pathology. - Wikidata - awgldk - TriplyDB

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

http://www.wikidata.org/entity/Q33510918

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Defining the extracellular matrix using proteomics Mechanisms and models of endoplasmic reticulum stress in chondrodysplasia Endoplasmic reticulum stress in chondrodysplasias caused by mutations in collagen types II and X Advances in Skeletal Dysplasia Genetics XBP1-Independent UPR Pathways Suppress C/EBP-β Mediated Chondrocyte Differentiation in ER-Stress Related Skeletal Disease Collagen XXVII organises the pericellular matrix in the growth plate An unfolded protein response is the initial cellular response to the expression of mutant matrilin-3 in a mouse model of multiple epiphyseal dysplasia.Genome-wide analyses of gene expression during mouse endochondral ossification Identification of key genes associated with Schmid-type metaphyseal chondrodysplasia based on microarray data.Silencing of both ATF4 and PERK inhibits cell cycle progression and promotes the apoptosis of differentiating chondrocytes.Transcriptional profiling of chondrodysplasia growth plate cartilage reveals adaptive ER-stress networks that allow survival but disrupt hypertrophy Chaperoning osteogenesis: new protein-folding disease paradigms.Increased classical endoplasmic reticulum stress is sufficient to reduce chondrocyte proliferation rate in the growth plate and decrease bone growth.Endoplasmic reticulum stress or mutation of an EF-hand Ca(2+)-binding domain directs the FKBP65 rotamase to an ERAD-based proteolysis The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review).Changes in the chondrocyte and extracellular matrix proteome during post-natal mouse cartilage development.Severe Extracellular Matrix Abnormalities and Chondrodysplasia in Mice Lacking Collagen Prolyl 4-Hydroxylase Isoenzyme II in Combination with a Reduced Amount of Isoenzyme I.XBP1S, a BMP2-inducible transcription factor, accelerates endochondral bone growth by activating GEP growth factor.A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.Effects of aging on articular cartilage homeostasis.Loss of matrilin 1 does not exacerbate the skeletal phenotype in a mouse model of multiple epiphyseal dysplasia caused by a Matn3 V194D mutation Matrix disruptions, growth, and degradation of cartilage with impaired sulfation.New therapeutic targets in rare genetic skeletal diseases.XBP1S associates with RUNX2 and regulates chondrocyte hypertrophy.Hypertrophic chondrocytes have a limited capacity to cope with increases in endoplasmic reticulum stress without triggering the unfolded protein response Thyroglobulin From Molecular and Cellular Biology to Clinical Endocrinology.ADAM17 controls endochondral ossification by regulating terminal differentiation of chondrocytes.ARCN1 Mutations Cause a Recognizable Craniofacial Syndrome Due to COPI-Mediated Transport Defects.A novel transgenic mouse model of growth plate dysplasia reveals that decreased chondrocyte proliferation due to chronic ER stress is a key factor in reduced bone growth.The unfolded protein response and its relevance to connective tissue diseases.The chondrocytic journey in endochondral bone growth and skeletal dysplasia.Environmental temperature impact on bone and cartilage growth.Extracellular matrix and developing growth plate.Evidence for activation of the unfolded protein response in collagen IV nephropathies C/EBP homologous protein drives pro-catabolic responses in chondrocytes.The unfolded protein response in skeletal development and homeostasis.EIF2S3 Mutations Associated with Severe X-Linked Intellectual Disability Syndrome MEHMO.Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases.Increased intracellular proteolysis reduces disease severity in an ER stress-associated dwarfism.The Chemical Chaperone, PBA, Reduces ER Stress and Autophagy and Increases Collagen IV α5 Expression in Cultured Fibroblasts From Men With X-Linked Alport Syndrome and Missense Mutations.

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Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

http://www.wikidata.org/entity/Q33510918

description

2009 nî lūn-bûn

@nan

2009 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

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Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

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Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

@nl

type

label

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

@ast

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

@en

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

@nl

prefLabel

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

@ast

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

@en

Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

@nl

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JOURNAL.PGEN.1000691

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Targeted induction of endoplasmic reticulum stress induces cartilage pathology.

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Ben McDermott

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Louise Kung

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Lynette Knowles

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M Helen Rajpar

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Mel Heeran

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Michael D Briggs

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Rachel Eardley

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Richard Poulsom

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P2860

ER stress-mediated apoptosis in a new mouse model of osteogenesis imperfecta

Decreased chondrocyte proliferation and dysregulated apoptosis in the cartilage growth plate are key features of a murine model of epiphyseal dysplasia caused by a matn3 mutation.

Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP

Amino acid substitutions of conserved residues in the carboxyl-terminal domain of the alpha 1(X) chain of type X collagen occur in two unrelated families with metaphyseal chondrodysplasia type Schmid

Signal integration in the endoplasmic reticulum unfolded protein response

A novel and highly conserved collagen (pro(alpha)1(XXVII)) with a unique expression pattern and unusual molecular characteristics establishes a new clade within the vertebrate fibrillar collagen family

Pseudoachondroplasia and multiple epiphyseal dysplasia: mutation review, molecular interactions, and genotype to phenotype correlations

Intracellular signaling by the unfolded protein response

A type X collagen mutation causes Schmid metaphyseal chondrodysplasia

A diastrophic dysplasia sulfate transporter (SLC26A2) mutant mouse: morphological and biochemical characterization of the resulting chondrodysplasia phenotype

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10.1371/JOURNAL.PGEN.1000691

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John F. Bateman

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2009-10-16T00:00:00Z

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38015801

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endoplasmic reticulum

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2757901

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