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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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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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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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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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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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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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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.6018-6028

2010

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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.3011-3024

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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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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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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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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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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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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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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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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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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Dual mode of activation of transcription by CBF, a physiological activator of the two type I collagen genes

Matrix biology, 1996-09, Vol.15 (3), p.192-192

1996

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Cartilage oligomeric matrix protein

AfCS-Nature Molecule Pages, 2010-11

2010

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Cultures of fibroblasts in fibrin lattices: Models for the study of metabolic activities of the cells in physiological conditions

Journal of cellular physiology, 1989-09, Vol.140 (3), p.483-490

1989

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

Identification of SOX9 interaction sites in the genome of chondrocytes

Resveratrol Reduces COMPopathy in Mice Through Activation of Autophagy

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

Cartilage oligomeric matrix protein: COMPopathies and beyond

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

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

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

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

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

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

D469del-COMP Retention in Chondrocytes Stimulates Caspase-Independent Necroptosis

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

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

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 (∗)

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

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

Dual mode of activation of transcription by CBF, a physiological activator of the two type I collagen genes

Cartilage oligomeric matrix protein

Cultures of fibroblasts in fibrin lattices: Models for the study of metabolic activities of the cells in physiological conditions

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