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Curcumin and Resveratrol: Nutraceuticals with so Much Potential for Pseudoachondroplasia and Other ER-Stress Conditions

Biomolecules (Basel, Switzerland), 2024-01, Vol.14 (2), p.154

Posey, Karen L

2024

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CurQ+, a Next-Generation Formulation of Curcumin, Ameliorates Growth Plate Chondrocyte Stress and Increases Limb Growth in a Mouse Model of Pseudoachondroplasia

International journal of molecular sciences, 2023-02, Vol.24 (4), p.3845

2023

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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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Cartilage oligomeric matrix protein: COMPopathies and beyond

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

2018

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Early Resveratrol Treatment Mitigates Joint Degeneration and Dampens Pain in a Mouse Model of Pseudoachondroplasia (PSACH)

Biomolecules (Basel, Switzerland), 2023-10, Vol.13 (10), p.1553

2023

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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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Skeletal Abnormalities in Mice Lacking Extracellular Matrix Proteins, Thrombospondin-1, Thrombospondin-3, Thrombospondin-5, and Type IX Collagen

The American journal of pathology, 2008-06, Vol.172 (6), p.1664-1674

2008

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Mutant COMP shapes growth and development of skull and facial structures in mice and humans

Molecular genetics & genomic medicine, 2020-07, Vol.8 (7), p.e1251-n/a

2020

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Health consequences of mutant cartilage oligomeric matrix protein and its relationship to abnormal growth and joint degeneration

Matrix biology, 2023-05, Vol.119, p.101-111

2023

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Novel therapeutic interventions for pseudoachondroplasia

Bone (New York, N.Y.), 2017-09, Vol.102, p.60-68

2017

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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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RNAi reduces expression and intracellular retention of mutant cartilage oligomeric matrix protein

PloS one, 2010-04, Vol.5 (4), p.e10302

2010

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Thrombospondins and Novel TSR-containing Proteins, R-spondins, Regulate Bone Formation and Remodeling

Current osteoporosis reports, 2010-06, Vol.8 (2), p.68-76

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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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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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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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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An Inducible Cartilage Oligomeric Matrix Protein Mouse Model Recapitulates Human Pseudoachondroplasia Phenotype

The American journal of pathology, 2009-10, Vol.175 (4), p.1555-1563

2009

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Assessing the plasticity of DNA target site recognition of the PI-SceI homing endonuclease using a bacterial two-hybrid selection system

Journal of molecular biology, 2003-12, Vol.334 (5), p.993-1008

2003

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COMP mutations: Domain-dependent relationship between abnormal chondrocyte trafficking and clinical PSACH and MED phenotypes

Journal of cellular biochemistry, 2008-02, Vol.103 (3), p.778-787

2008

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Role of TSP-5/COMP in Pseudoachondroplasia

The international journal of biochemistry & cell biology, 2004-06, Vol.36 (6), p.1005-1012

2004

Volltextzugriff (PDF)

Evolution of divergent DNA recognition specificities in VDE homing endonucleases from two yeast species

Nucleic acids research, 2004-01, Vol.32 (13), p.3947

2004

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Curcumin and Resveratrol: Nutraceuticals with so Much Potential for Pseudoachondroplasia and Other ER-Stress Conditions

CurQ+, a Next-Generation Formulation of Curcumin, Ameliorates Growth Plate Chondrocyte Stress and Increases Limb Growth in a Mouse Model of Pseudoachondroplasia

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

Cartilage oligomeric matrix protein: COMPopathies and beyond

Early Resveratrol Treatment Mitigates Joint Degeneration and Dampens Pain in a Mouse Model of Pseudoachondroplasia (PSACH)

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

Resveratrol Reduces COMPopathy in Mice Through Activation of Autophagy

Skeletal Abnormalities in Mice Lacking Extracellular Matrix Proteins, Thrombospondin-1, Thrombospondin-3, Thrombospondin-5, and Type IX Collagen

Mutant COMP shapes growth and development of skull and facial structures in mice and humans

Health consequences of mutant cartilage oligomeric matrix protein and its relationship to abnormal growth and joint degeneration

Novel therapeutic interventions for pseudoachondroplasia

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

RNAi reduces expression and intracellular retention of mutant cartilage oligomeric matrix protein

Thrombospondins and Novel TSR-containing Proteins, R-spondins, Regulate Bone Formation and Remodeling

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

Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology

D469del-COMP Retention in Chondrocytes Stimulates Caspase-Independent Necroptosis

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

An Inducible Cartilage Oligomeric Matrix Protein Mouse Model Recapitulates Human Pseudoachondroplasia Phenotype

Assessing the plasticity of DNA target site recognition of the PI-SceI homing endonuclease using a bacterial two-hybrid selection system

COMP mutations: Domain-dependent relationship between abnormal chondrocyte trafficking and clinical PSACH and MED phenotypes

Role of TSP-5/COMP in Pseudoachondroplasia

Evolution of divergent DNA recognition specificities in VDE homing endonucleases from two yeast species

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