ArticleScientific reports2019
Overlapping and differential functions of ATF6α versus ATF6β in the mouse heart.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- QRICH1 regulates ATF6 transcription to affect pathological cardiac hypertrophy progression.Molecular medicine (Cambridge, Mass.) · 2025Article
- Homeostasis control in health and disease by the unfolded protein response.Nature reviews. Molecular cell biology · 2025Review
- Review
- Article
- 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
- Competing endogenous RNAs in human astrocytes: crosstalk and interacting networks in response to lipotoxicity.Frontiers in neuroscience · 2023Article
- Normal tissue homeostasis and impairment of selective inflammatory responses in dendritic cells deficient for ATF6α.Frontiers in cell and developmental biology · 2023Article
- The regulatory role of endoplasmic reticulum chaperone proteins in neurodevelopment.Frontiers in neuroscience · 2022Review
- Newly synthesized mRNA escapes translational repression during the acute phase of the mammalian unfolded protein response.PloS one · 2022Article
- Thbs1 induces lethal cardiac atrophy through PERK-ATF4 regulated autophagy.Nature communications · 2021Article
- The ATF6β-calreticulin axis promotes neuronal survival under endoplasmic reticulum stress and excitotoxicity.Scientific reports · 2021Article
- Endoplasmic reticulum stress, cell death and tumor: Association between endoplasmic reticulum stress and the apoptosis pathway in tumors (Review).Oncology reports · 2021Review
- Endoplasmic reticulum stress serves an important role in cardiac ischemia/reperfusion injury (Review).Experimental and therapeutic medicine · 2020Review
- A pilot study on gene expression of endoplasmic reticulum unfolded protein response in chronic kidney disease.Biochemistry and biophysics reports · 2020Article
- Regulation of autophagy by canonical and non-canonical ER stress responses.Seminars in cancer biology · 2020Review
- Intersection of the ATF6 and XBP1 ER stress pathways in mouse islet cells.The Journal of biological chemistry · 2020Article
- Differentially expressed lncRNAs, miRNAs and mRNAs with associated ceRNA networks in a mouse model of myocardial ischemia/reperfusion injury.Molecular medicine reports · 2020Article
- Transcription factors activated through RIP (regulated intramembrane proteolysis) and RAT (regulated alternative translocation).The Journal of biological chemistry · 2020Review
- Calreticulin expression in human cardiac myocytes induces ER stress-associated apoptosis.Physiological reports · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Hemodynamic stress on the mammalian heart results in compensatory hypertrophy and activation of the unfolded protein response through activating transcription factor 6α (ATF6α) in cardiac myocytes, but the roles of ATF6α or the related transcription factor ATF6β in regulating this hypertrophic response are not well-understood. Here we examined the effects of loss of ATF6α or ATF6β on the cardiac response to pressure overload. Mice gene-deleted for Atf6 or Atf6b were subjected to 2 weeks of transverse aortic constriction, and each showed a significant reduction in hypertrophy with reduced expression of endoplasmic reticulum (ER) stress-associated proteins compared with controls. However, with long-term pressure overload both Atf6 and Atf6b null mice showed enhanced decompensation typified by increased heart weight, pulmonary edema and reduced function compared to control mice. Our subsequent studies using cardiac-specific transgenic mice expressing the transcriptionally active N-terminus of ATF6α or ATF6β revealed that these factors control overlapping gene expression networks that include numerous ER protein chaperones and ER associated degradation components. This work reveals previously unappreciated roles for ATF6α and ATF6β in regulating the pressure overload induced cardiac hypertrophic response and in controlling the expression of genes that condition the ER during hemodynamic stress.
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Registered trials
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