ArticleBiochemical and biophysical research communications2014
Synthetic embryonic lethality upon deletion of the ER cochaperone p58(IPK) and the ER stress sensor ATF6α.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Gut microbiota modulate intestinal inflammation by endoplasmic reticulum stress-autophagy-cell death signaling axis.Journal of animal science and biotechnology · 2025Review
- OTUB1 facilitates bladder cancer progression by stabilizing ATF6 in response to endoplasmic reticulum stress.Cancer science · 2021Article
- Type I interferons and endoplasmic reticulum stress in health and disease.International review of cell and molecular biology · 2020Review
- Endoplasmic Reticulum Stress and Intestinal Inflammation: A Perilous Union.Frontiers in immunology · 2020Review
- ER Stress and the UPR in Shaping Intestinal Tissue Homeostasis and Immunity.Frontiers in immunology · 2019Review
- ER Stress Inhibits Liver Fatty Acid Oxidation while Unmitigated Stress Leads to Anorexia-Induced Lipolysis and Both Liver and Kidney Steatosis.Cell reports · 2017Article
- Overexpression of p58ipk protects neuroblastoma against paraquat-induced toxicity.International journal of clinical and experimental pathology · 2017Article
- Expression and regulation of ATF6α in the mouse uterus during embryo implantation.Reproductive biology and endocrinology : RB&E · 2016Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The unfolded protein response (UPR) is activated as a consequence of alterations to ER homeostasis. It upregulates a group of ER chaperones and cochaperones, as well as other genes that improve protein processing within the secretory pathway. The UPR effector ATF6α augments-but is not essential for-maximal induction of ER chaperones during stress, yet its role, if any, in protecting cellular function during normal development and physiology is unknown. A systematic analysis of multiple tissues from Atf6α-/- mice revealed that all tissues examined were grossly insensitive to loss of ATF6α. However, combined deletion of ATF6α and the ER cochaperone p58(IPK) resulted in synthetic embryonic lethality. These findings reveal for the first time that an intact UPR can compensate for the genetic impairment of protein folding in the ER in vivo. The also expose a role for p58(IPK) in normal embryonic development.
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