ReviewCell stress & chaperones2016
Endoplasmic reticulum stress in chondrodysplasias caused by mutations in collagen types II and X.
Review in Cell stress & chaperones, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- COL12A1 rs970547 Polymorphism Predisposes Anterior Cruciate Ligament Injury by Inducing ER Stress and Impairing Fibroblast Function.Advanced biology · 2026Article
- Exploring the clinical and genetic spectrum of Steel syndrome: two case reports and review of the literature.Frontiers in medicine · 2026Article
- CRISPR-Mediated Endogenous Activation of Fibroin Heavy Chain Gene Triggers Cellular Stress Responses inInsects · 2021Article
- Maturation of the equine medial femoral condyle osteochondral unit.Osteoarthritis and cartilage open · 2020Article
- Suppressing UPR-dependent overactivation of FGFR3 signaling ameliorates SLC26A2-deficient chondrodysplasias.EBioMedicine · 2019Article
- 4-PBA ameliorates cellular homeostasis in fibroblasts from osteogenesis imperfecta patients by enhancing autophagy and stimulating protein secretion.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Different Forms of ER Stress in Chondrocytes Result in Short Stature Disorders and Degenerative Cartilage Diseases: New Insights by Cartilage-Specific ERp57 Knockout Mice.Oxidative medicine and cellular longevity · 2018Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endoplasmic reticulum is primarily recognized as the site of synthesis and folding of secreted, membrane-bound, and some organelle-targeted proteins. An imbalance between the load of unfolded proteins and the processing capacity in endoplasmic reticulum leads to the accumulation of unfolded or misfolded proteins and endoplasmic reticulum stress, which is a hallmark of a number of storage diseases, including neurodegenerative diseases, a number of metabolic diseases, and cancer. Moreover, its contribution as a novel mechanistic paradigm in genetic skeletal diseases associated with abnormalities of the growth plates and dwarfism is considered. In this review, I discuss the mechanistic significance of endoplasmic reticulum stress, abnormal folding, and intracellular retention of mutant collagen types II and X in certain variants of skeletal chondrodysplasia.
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