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INFLUENCE DE LA MATRICE EXTRACELLULAIRE SUR LES CARACTERES PHENOTYPIQUES DES FIBROBLASTES EN CULTURE

Reproduction, nutrition, development, 1989, Vol.29 (Suppl), p.39-39

1989

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Cartilage oligomeric matrix protein: COMPopathies and beyond

Matrix biology, 2018-10, Vol.71-72, p.161-173

2018

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Constitutive Activation of MKK6 in Chondrocytes of Transgenic Mice Inhibits Proliferation and Delays Endochondral Bone Formation

Proceedings of the National Academy of Sciences - PNAS, 2006-01, Vol.103 (2), p.365-370

2006

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The dimerization domain of SOX9 is required for transcription activation of a chondrocyte-specific chromatin DNA template

Nucleic acids research, 2010-10, Vol.38 (18), p.6018

2010

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Joint Degeneration in a Mouse Model of Pseudoachondroplasia: ER Stress, Inflammation, and Block of Autophagy

International journal of molecular sciences, 2021-09, Vol.22 (17), p.9239

2021

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D469del-COMP Retention in Chondrocytes Stimulates Caspase-Independent Necroptosis

The American journal of pathology, 2012-02, Vol.180 (2), p.738-748

2012

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Primary Osteoarthritis Early Joint Degeneration Induced by Endoplasmic Reticulum Stress Is Mitigated by Resveratrol

The American journal of pathology, 2021-09, Vol.191 (9), p.1624-1637

2021

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Identification of SOX9 interaction sites in the genome of chondrocytes

PloS one, 2010-04, Vol.5 (4), p.e10113-e10113

2010

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Chondrocyte‐Specific Pathology During Skeletal Growth and Therapeutics in a Murine Model of Pseudoachondroplasia

Journal of bone and mineral research, 2014-05, Vol.29 (5), p.1258-1268

2014

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Resveratrol Reduces COMPopathy in Mice Through Activation of Autophagy

JBMR plus, 2021-03, Vol.5 (3), p.e10456-n/a

2021

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Antioxidant and anti-inflammatory agents mitigate pathology in a mouse model of pseudoachondroplasia

Human molecular genetics, 2015-07, Vol.24 (14), p.3918-3928

2015

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Novel mTORC1 Mechanism Suggests Therapeutic Targets for COMPopathies

The American journal of pathology, 2019-01, Vol.189 (1), p.132-146

2019

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Mutant cartilage oligomeric matrix protein (COMP) compromises bone integrity, joint function and the balance between adipogenesis and osteogenesis

Matrix biology, 2018-04, Vol.67, p.75-89

2018

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Transcriptional regulation of chondrogenesis by coactivator Tip60 via chromatin association with Sox9 and Sox5

Nucleic acids research, 2008-05, Vol.36 (9), p.3011

2008

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Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology

Molecular therapy, 2017-03, Vol.25 (3), p.705-714

2017

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DNA Binding Specificity of the CCAAT-binding Factor CBF/NF-Y

The Journal of biological chemistry, 1997-10, Vol.272 (42), p.26562-26572

1997

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Chop (Ddit3) Is Essential for D469del-COMP Retention and Cell Death in Chondrocytes in an Inducible Transgenic Mouse Model of Pseudoachondroplasia

The American journal of pathology, 2012-02, Vol.180 (2), p.727-737

2012

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The Transcriptional Activity of the CCAAT-binding Factor CBF Is Mediated by Two Distinct Activation Domains, One in the CBF-B Subunit and the Other in the CBF-C Subunit

The Journal of biological chemistry, 1996-06, Vol.271 (24), p.14485-14491

1996

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CBF/NF-Y Functions Both in Nucleosomal Disruption and Transcription Activation of the Chromatin-assembled Topoisomerase II alpha Promoter: TRANSCRIPTION ACTIVATION BY CBF/NF-Y IN CHROMATIN IS DEPENDENT ON THE PROMOTER STRUCTURE

The Journal of biological chemistry, 2001-11, Vol.276 (44), p.40621-40630

2001

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Studies on Transcription Activation by the Multimeric CCAAT-binding Factor CBF (∗)

The Journal of biological chemistry, 1995-01, Vol.270 (1), p.468-475

1995

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Role of UPR in the retention of mutant COMP in PSACH chondrocytes

Matrix biology, 2008-12, Vol.27, p.52-52

2008

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The two activation domains of the CCAAT-binding factor CBF interact with the dTAFII110 component of the Drosophila TFIID complex

Biochemical journal, 1998-04, Vol.331 ( Pt 1) (1), p.291-297

1998

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CBF/NF-Y functions both in nucleosomal disruption and transcription activation of the chromatin-assembled topoisomerase IIalpha promoter. Transcription activation by CBF/NF-Y in chromatin is dependent on the promoter structure

The Journal of biological chemistry, 2001-11, Vol.276 (44), p.40621-40630

2001

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CBF/NF-Y Functions Both in Nucleosomal Disruption and Transcription Activation of the Chromatin-assembled Topoisomerase IIα Promoter

The Journal of biological chemistry, 2001-11, Vol.276 (44), p.40621-40630

2001

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CBF/NF-Y Functions Both in Nucleosomal Disruption and Transcription Activation of the Chromatin-assembled Topoisomerase IIÎ± Promoter

The Journal of biological chemistry, 2001-11, Vol.276 (44), p.40621

2001

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Chondrocytes - Metabolism
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Biological And Medical Sciences
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Cartilage
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Chondrocytes
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Cartilage Oligomeric Matrix Protein - Genetics
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Cells, Cultured
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Pathology
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Achondroplasia - Genetics
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Cartilage Oligomeric Matrix Protein
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INFLUENCE DE LA MATRICE EXTRACELLULAIRE SUR LES CARACTERES PHENOTYPIQUES DES FIBROBLASTES EN CULTURE

Cartilage oligomeric matrix protein: COMPopathies and beyond

Constitutive Activation of MKK6 in Chondrocytes of Transgenic Mice Inhibits Proliferation and Delays Endochondral Bone Formation

The dimerization domain of SOX9 is required for transcription activation of a chondrocyte-specific chromatin DNA template

Joint Degeneration in a Mouse Model of Pseudoachondroplasia: ER Stress, Inflammation, and Block of Autophagy

D469del-COMP Retention in Chondrocytes Stimulates Caspase-Independent Necroptosis

Primary Osteoarthritis Early Joint Degeneration Induced by Endoplasmic Reticulum Stress Is Mitigated by Resveratrol

Identification of SOX9 interaction sites in the genome of chondrocytes

Chondrocyte‐Specific Pathology During Skeletal Growth and Therapeutics in a Murine Model of Pseudoachondroplasia

Resveratrol Reduces COMPopathy in Mice Through Activation of Autophagy

Antioxidant and anti-inflammatory agents mitigate pathology in a mouse model of pseudoachondroplasia

Novel mTORC1 Mechanism Suggests Therapeutic Targets for COMPopathies

Mutant cartilage oligomeric matrix protein (COMP) compromises bone integrity, joint function and the balance between adipogenesis and osteogenesis

Transcriptional regulation of chondrogenesis by coactivator Tip60 via chromatin association with Sox9 and Sox5

Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology

DNA Binding Specificity of the CCAAT-binding Factor CBF/NF-Y

Chop (Ddit3) Is Essential for D469del-COMP Retention and Cell Death in Chondrocytes in an Inducible Transgenic Mouse Model of Pseudoachondroplasia

The Transcriptional Activity of the CCAAT-binding Factor CBF Is Mediated by Two Distinct Activation Domains, One in the CBF-B Subunit and the Other in the CBF-C Subunit

CBF/NF-Y Functions Both in Nucleosomal Disruption and Transcription Activation of the Chromatin-assembled Topoisomerase II alpha Promoter: TRANSCRIPTION ACTIVATION BY CBF/NF-Y IN CHROMATIN IS DEPENDENT ON THE PROMOTER STRUCTURE

Studies on Transcription Activation by the Multimeric CCAAT-binding Factor CBF (∗)

Role of UPR in the retention of mutant COMP in PSACH chondrocytes

The two activation domains of the CCAAT-binding factor CBF interact with the dTAFII110 component of the Drosophila TFIID complex

CBF/NF-Y functions both in nucleosomal disruption and transcription activation of the chromatin-assembled topoisomerase IIalpha promoter. Transcription activation by CBF/NF-Y in chromatin is dependent on the promoter structure

CBF/NF-Y Functions Both in Nucleosomal Disruption and Transcription Activation of the Chromatin-assembled Topoisomerase IIα Promoter

CBF/NF-Y Functions Both in Nucleosomal Disruption and Transcription Activation of the Chromatin-assembled Topoisomerase IIÎ± Promoter

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