Increased Classical Endoplasmic Reticulum Stress Is Sufficient to Reduce Chondrocyte Proliferation Rate in the Growth Plate and Decrease Bone Growth

Mechanisms and models of endoplasmic reticulum stress in chondrodysplasia

(2014) Sara E. Patterson et al.   DEVELOPMENTAL DYNAMICS

Abnormal Chondrocyte Apoptosis in the Cartilage Growth Plate is Influenced by Genetic Background and Deletion of CHOP in a Targeted Mouse Model of Pseudoachondroplasia

(2014) Katarzyna A. Piróg et al.   PLoS One

Endoplasmic Reticulum Stress-Unfolding Protein Response-Apoptosis Cascade Causes Chondrodysplasia in a col2a1 p.Gly1170Ser Mutated Mouse Model

(2014) Guoyan Liang et al.   PLoS One

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

(2013) B. Gualeni et al.   Disease Models & Mechanisms

Development of the Endochondral Skeleton

(2013) F. Long et al.   Cold Spring Harbor Perspectives in Biology

Analysis of the cartilage proteome from three different mouse models of genetic skeletal diseases reveals common and discrete disease signatures

(2013) P. A. Bell et al.   Biology Open

Hypertrophic Chondrocytes Have a Limited Capacity to Cope with Increases in Endoplasmic Reticulum Stress without Triggering the Unfolded Protein Response

(2012) Louise H. W. Kung et al.   JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY

Nosology and classification of genetic skeletal disorders: 2010 revision

(2011) Matthew L. Warman et al.   AMERICAN JOURNAL OF MEDICAL GENETICS PART A

A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia

(2011) Farhana Suleman et al.   HUMAN MUTATION

The skeleton: a multi-functional complex organ. The growth plate chondrocyte and endochondral ossification

(2011) E J Mackie et al.   JOURNAL OF ENDOCRINOLOGY

ENU-induced missense mutation in the C-propeptide coding region of Col2a1 creates a mouse model of platyspondylic lethal skeletal dysplasia, Torrance type

(2011) Tatsuya Furuichi et al.   MAMMALIAN GENOME

Transcriptional Profiling of Chondrodysplasia Growth Plate Cartilage Reveals Adaptive ER-Stress Networks That Allow Survival but Disrupt Hypertrophy

(2011) Trevor L. Cameron et al.   PLoS One

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

(2010) Seema Nundlall et al.   CELL STRESS & CHAPERONES

Molecular chaperones and substrate ubiquitination control the efficiency of endoplasmic reticulum-associated degradation

(2010) J. L. Goeckeler et al.   DIABETES OBESITY & METABOLISM

Endoplasmic Reticulum Stress Response Mediated by the PERK-eIF2α-ATF4 Pathway Is Involved in Osteoblast Differentiation Induced by BMP2

(2010) Atsushi Saito et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

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

(2009) Karen L. Posey et al.   AMERICAN JOURNAL OF PATHOLOGY

The unfolded protein response and its relevance to connective tissue diseases

(2009) Raymond P. Boot-Handford et al.   CELL AND TISSUE RESEARCH

Regulation of endoplasmic reticulum stress response by a BBF2H7-mediated Sec23a pathway is essential for chondrogenesis

(2009) Atsushi Saito et al.   NATURE CELL BIOLOGY

Targeted Induction of Endoplasmic Reticulum Stress Induces Cartilage Pathology

(2009) M. Helen Rajpar et al.   PLoS Genetics

Thrombospondins: from structure to therapeutics

(2008) K. L. Posey et al.   CELLULAR AND MOLECULAR LIFE SCIENCES

Endoplasmic Reticulum (ER) Chaperone Regulation and Survival of Cells Compensating for Deficiency in the ER Stress Response Kinase, PERK

(2008) Yukihiro Yamaguchi et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

PERK is essential for neonatal skeletal development to regulate osteoblast proliferation and differentiation

(2008) Jianwen Wei et al.   JOURNAL OF CELLULAR PHYSIOLOGY

Endochondral ossification: How cartilage is converted into bone in the developing skeleton

(2007) E.J. Mackie et al.   INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY

Transgenic mice expressing D469Δ mutated cartilage oligomeric matrix protein (COMP) show growth plate abnormalities and sternal malformations

(2007) Markus Schmitz et al.   MATRIX BIOLOGY