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The aggrecanopathies; an evolving phenotypic spectrum of human genetic skeletal diseases

Orphanet journal of rare diseases, 2016-06, Vol.11 (1), p.86-86, Article 86

2016

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CRELD2 is a novel modulator of calcium release and calcineurin-NFAT signalling during osteoclast differentiation

Scientific reports, 2022-08, Vol.12 (1), p.13884-13884, Article 13884

2022

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Multiple epiphyseal dysplasia and related disorders: Molecular genetics, disease mechanisms, and therapeutic avenues

Developmental dynamics, 2021-03, Vol.250 (3), p.345-359

2021

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Curcumin Reduces Pathological Endoplasmic Reticulum Stress through Increasing Proteolysis of Mutant Matrilin-3

International journal of molecular sciences, 2023-01, Vol.24 (2), p.1496

2023

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unfolded protein response and its relevance to connective tissue diseases

Cell and tissue research, 2010-01, Vol.339 (1), p.197-211

2010

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Increased classical endoplasmic reticulum stress is sufficient to reduce chondrocyte proliferation rate in the growth plate and decrease bone growth

PloS one, 2015-02, Vol.10 (2), p.e0117016-e0117016

2015

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Increased intracellular proteolysis reduces disease severity in an ER stress-associated dwarfism

The Journal of clinical investigation, 2017-10, Vol.127 (10), p.3861-3865

2017

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Cartilage endoplasmic reticulum stress may influence the onset but not the progression of experimental osteoarthritis

Arthritis research & therapy, 2019-09, Vol.21 (1), p.206-13, Article 206

2019

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Targeted induction of endoplasmic reticulum stress induces cartilage pathology

PLoS genetics, 2009-10, Vol.5 (10), p.e1000691-e1000691

2009

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Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases

Human molecular genetics, 2013-12, Vol.22 (25), p.5262-5275

2013

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XBP1 signalling is essential for alleviating mutant protein aggregation in ER-stress related skeletal disease

PLoS genetics, 2019-07, Vol.15 (7), p.e1008215-e1008215

2019

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Genotype to phenotype correlations in cartilage oligomeric matrix protein associated chondrodysplasias

European journal of human genetics : EJHG, 2014-11, Vol.22 (11), p.1278-1282

2014

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Increased hippocampal excitability in miR-324-null mice

Scientific reports, 2021-05, Vol.11 (1), p.10452-10452, Article 10452

2021

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Abnormal chondrocyte apoptosis in the cartilage growth plate is influenced by genetic background and deletion of CHOP in a targeted mouse model of pseudoachondroplasia

PloS one, 2014-02, Vol.9 (2), p.e85145-e85145

2014

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Collagen XXVII organises the pericellular matrix in the growth plate

PloS one, 2011-12, Vol.6 (12), p.e29422-e29422

2011

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New developments in chondrocyte ER stress and related diseases [version 1; peer review: 2 approved]

F1000 research, 2020, Vol.9, p.290

2020

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Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases

PloS one, 2013-11, Vol.8 (11), p.e82412-e82412

2013

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New therapeutic targets in rare genetic skeletal diseases

Expert opinion on orphan drugs, 2015-10, Vol.3 (10), p.1137-1154

2015

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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

Cell stress & chaperones, 2010-11, Vol.15 (6), p.835-849

2010

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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

Human molecular genetics, 2007-07, Vol.16 (14), p.1728-1741

2007

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Collagen XXVII Is Developmentally Regulated and Forms Thin Fibrillar Structures Distinct from Those of Classical Vertebrate Fibrillar Collagens

The Journal of biological chemistry, 2007-04, Vol.282 (17), p.12791-12795

2007

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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

Disease models & mechanisms, 2013-11, Vol.6 (6), p.1414-1425

2013

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Structural and Functional Characterization of Recombinant Matrilin-3 A-domain and Implications for Human Genetic Bone Diseases

The Journal of biological chemistry, 2007-11, Vol.282 (48), p.34634-34643

2007

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CRELD2 Is a Novel LRP1 Chaperone That Regulates Noncanonical WNT Signaling in Skeletal Development

Journal of bone and mineral research, 2020-08, Vol.35 (8), p.1452-1469

2020

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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)

International journal of molecular medicine, 2015-06, Vol.35 (6), p.1483-1492

2015

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The aggrecanopathies; an evolving phenotypic spectrum of human genetic skeletal diseases

CRELD2 is a novel modulator of calcium release and calcineurin-NFAT signalling during osteoclast differentiation

Multiple epiphyseal dysplasia and related disorders: Molecular genetics, disease mechanisms, and therapeutic avenues

Curcumin Reduces Pathological Endoplasmic Reticulum Stress through Increasing Proteolysis of Mutant Matrilin-3

unfolded protein response and its relevance to connective tissue diseases

Increased classical endoplasmic reticulum stress is sufficient to reduce chondrocyte proliferation rate in the growth plate and decrease bone growth

Increased intracellular proteolysis reduces disease severity in an ER stress-associated dwarfism

Cartilage endoplasmic reticulum stress may influence the onset but not the progression of experimental osteoarthritis

Targeted induction of endoplasmic reticulum stress induces cartilage pathology

Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases

XBP1 signalling is essential for alleviating mutant protein aggregation in ER-stress related skeletal disease

Genotype to phenotype correlations in cartilage oligomeric matrix protein associated chondrodysplasias

Increased hippocampal excitability in miR-324-null mice

Abnormal chondrocyte apoptosis in the cartilage growth plate is influenced by genetic background and deletion of CHOP in a targeted mouse model of pseudoachondroplasia

Collagen XXVII organises the pericellular matrix in the growth plate

New developments in chondrocyte ER stress and related diseases [version 1; peer review: 2 approved]

Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases

New therapeutic targets in rare genetic skeletal diseases

An unfolded protein response is the initial cellular response to the expression of mutant matrilin-3 in a mouse model of multiple epiphyseal dysplasia

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

Collagen XXVII Is Developmentally Regulated and Forms Thin Fibrillar Structures Distinct from Those of Classical Vertebrate Fibrillar Collagens

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

Structural and Functional Characterization of Recombinant Matrilin-3 A-domain and Implications for Human Genetic Bone Diseases

CRELD2 Is a Novel LRP1 Chaperone That Regulates Noncanonical WNT Signaling in Skeletal Development

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)

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