ArticleMolecular biology of the cell2013
ATF6α/β-mediated adjustment of ER chaperone levels is essential for development of the notochord in medaka fish.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
- Collagen Biosynthesis and Its Molecular Ensemble: What Remains Unexplored.Biochemistry · 2025Review
- Impact of ATF6 deletion on the embryonic brain development.iScience · 2025Article
- BiP, GRP94, calreticulin and calnexin contribute to development of the notochord in medaka fish.Cell structure and function · 2025Article
- Tango1L but not Tango1S, Tali and cTAGE5 is required for export of type II collagen in medaka fish.Cell structure and function · 2025Article
- Gene module reconstruction identifies cellular differentiation processes and the regulatory logic of specialized secretion in zebrafish.Developmental cell · 2025Article
- Vesicular trafficking and cell-cell communication in neurodevelopment and neurodegeneration.Frontiers in cell and developmental biology · 2025Review
- Protective effect of CK2 against endoplasmic reticulum stress in pancreatic β cells.Diabetology international · 2025Article
- Essential roles of the unfolded protein response in intestinal physiology.eGastroenterology · 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
- Article
- Activation of XBP1 but not ATF6α rescues heart failure induced by persistent ER stress in medaka fish.Life science alliance · 2023Article
- Loss of ATF6α in a human carcinoma cell line is compensated not by its paralogue ATF6β but by sustained activation of the IRE1 and PERK arms for tumor growth in nude mice.Molecular biology of the cell · 2023Article
- Evolutionary Aspects of the Unfolded Protein Response.Cold Spring Harbor perspectives in biology · 2022Article
- Scleral PERK and ATF6 as targets of myopic axial elongation of mouse eyes.Nature communications · 2022Article
- The ATF6β-calreticulin axis promotes neuronal survival under endoplasmic reticulum stress and excitotoxicity.Scientific reports · 2021Article
- Collagen's enigmatic, highly conservedProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Reinvestigation of Disulfide-bonded Oligomeric Forms of the Unfolded Protein Response Transducer ATF6.Cell structure and function · 2020Article
- Active receptor tyrosine kinases, but not Brachyury, are sufficient to trigger chordoma in zebrafish.Disease models & mechanisms · 2019Article
- The unfolded protein response in metazoan development.Journal of cell science · 2019Review
- Roles of the endoplasmic reticulum-resident, collagen-specific molecular chaperone Hsp47 in vertebrate cells and human disease.The Journal of biological chemistry · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATF6α and ATF6β are membrane-bound transcription factors activated by regulated intramembrane proteolysis in response to endoplasmic reticulum (ER) stress to induce various ER quality control proteins. ATF6α- and ATF6β single-knockout mice develop normally, but ATF6α/β double knockout causes embryonic lethality, the reason for which is unknown. Here we show in medaka fish that ATF6α is primarily responsible for transcriptional induction of the major ER chaperone BiP and that ATF6α/β double knockout, but not ATF6α- or ATF6β single knockout, causes embryonic lethality, as in mice. Analyses of ER stress reporters reveal that ER stress occurs physiologically during medaka early embryonic development, particularly in the brain, otic vesicle, and notochord, resulting in ATF6α- and ATF6β-mediated induction of BiP, and that knockdown of the α1 chain of type VIII collagen reduces such ER stress. The absence of transcriptional induction of several ER chaperones in ATF6α/β double knockout causes more profound ER stress and impaired notochord development, which is partially rescued by overexpression of BiP. Thus ATF6α/β-mediated adjustment of chaperone levels to increased demands in the ER is essential for development of the notochord, which synthesizes and secretes large amounts of extracellular matrix proteins to serve as the body axis before formation of the vertebra.
Indexed as
Identifiers
What OpenQuestion holds
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.