ArticleMatrix biology : journal of the International Society for Matrix Biology2018
Paradoxical roles of ATF6α and ATF6β in modulating disease severity caused by mutations in collagen X.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed.
- Enhanced membrane protein production in HEK293T cells viaBiomolecules & biomedicine · 2025Article
- CREB3L1 deficiency impairs odontoblastic differentiation and molar dentin deposition partially through the TMEM30B.International journal of oral science · 2024Article
- Endoplasmic reticulum stress in diseases.MedComm · 2024Review
- RNASeq highlights ATF6 pathway regulators for CHO cell engineering with different impacts of ATF6β and WFS1 knockdown on fed-batch production of IgGScientific reports · 2024Article
- Review
- Genetic associations in ankylosing spondylitis: circulating proteins as drug targets and biomarkers.Frontiers in immunology · 2024Article
- Reciprocal negative feedback regulation of ATF6α and PTEN promotes prostate cancer progression.Cellular and molecular life sciences : CMLS · 2023Article
- Endoplasmic Reticulum Stress in Elderly Patients with COVID-19: Potential of Melatonin Treatment.Viruses · 2023Review
- ATF6α contributes to rheumatoid arthritis by inducing inflammatory cytokine production and apoptosis resistance.Frontiers in immunology · 2022Article
- Endoplasmic Reticulum Stress Signaling and the Pathogenesis of Hepatocarcinoma.International journal of molecular sciences · 2021Review
- Variants inBrain communications · 2021Article
- Endoplasmic Reticulum Stress and Tumor Microenvironment in Bladder Cancer: The Missing Link.Frontiers in cell and developmental biology · 2021Review
- Small molecule strategies to harness the unfolded protein response: where do we go from here?The Journal of biological chemistry · 2020Review
- Transcription factors activated through RIP (regulated intramembrane proteolysis) and RAT (regulated alternative translocation).The Journal of biological chemistry · 2020Review
- Crosstalk between ER stress, NLRP3 inflammasome, and inflammation.Applied microbiology and biotechnology · 2020Review
- Sledgehammer to Scalpel: Broad Challenges to the Heart and Other Tissues Yield Specific Cellular Responses via Transcriptional Regulation of the ER-Stress Master Regulator ATF6α.International journal of molecular sciences · 2020Review
- Review
- New developments in chondrocyte ER stress and related diseases.F1000Research · 2020Review
- Identification of two novel COL10A1 heterozygous mutations in two Chinese pedigrees with Schmid-type metaphyseal chondrodysplasia.BMC medical genetics · 2019Article
- Cartilage endoplasmic reticulum stress may influence the onset but not the progression of experimental osteoarthritis.Arthritis research & therapy · 2019Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Whilst the role of ATF6α in modulating the unfolded protein response (UPR) has been well documented, the function of its paralogue ATF6β is less well understood. Using knockdown in cell culture and gene ablation in mice we have directly compared the roles of ATF6α & β in responding to the increased ER stress induced by mutant forms of type X collagen that cause the ER stress-associated metaphyseal chondrodysplasia type Schmid (MCDS). ATF6α more efficiently deals with the disease-associated ER stress in the absence of ATF6β and conversely, ATF6β is less effective in the absence of ATF6α. Furthermore, disease severity in vivo is increased by ATF6α ablation and decreased by ATF6β ablation. In addition, novel functions for each paralogue are described including an ATF6β-specific role in controlling growth plate chondrocyte proliferation. The clear demonstration of the intimate relationship of the two ATF6 isoforms and how ATF6β can moderate the activity of ATF6α and vice versa is of great significance for understanding the UPR mechanism. The activities of both ATF6 isoforms and their separate roles need consideration when deciding how to target increased ER stress as a means of treating MCDS and other ER stress-associated diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.