ArticleThe Journal of cell biology2019
BIK ubiquitination by the E3 ligase Cul5-ASB11 determines cell fate during cellular stress.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Enterocytes rely on purine biosynthesis/salvage pathway to facilitate dietary fat absorption.Nature communications · 2026Article
- Targeting the unfolded protein response in cancer: mechanisms, small-molecule inhibitors, and translational challenges.Frontiers in immunology · 2026Review
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- BIK polymorphism and proteasome regulation unveil host risk factor for severe influenza.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigallocatechin gallate attenuated high glucose-induced pancreatic beta cell dysfunction by modulating DRP1-mediated mitochondrial apoptosis pathways.Scientific reports · 2024Article
- Bik promotes proteasomal degradation to control low-grade inflammation.The Journal of clinical investigation · 2023Article
- Broadening horizons: the contribution of mitochondria-associated endoplasmic reticulum membrane (MAM) dysfunction in diabetic kidney disease.International journal of biological sciences · 2023Review
- UBXD8 mediates mitochondria-associated degradation to restrain apoptosis and mitophagy.EMBO reports · 2022Article
- ASB17 Facilitates the Burst of LPS-Induced Inflammation Through Maintaining TRAF6 Stability.Frontiers in cellular and infection microbiology · 2022Article
- Shared Gene Expression and Immune Pathway Changes Associated with Progression from Nevi to Melanoma.Cancers · 2021Article
- E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1.Biology · 2021Article
- DNA damage promotes ER stress resistance through elevation of unsaturated phosphatidylcholine in Caenorhabditis elegans.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The BH3-only pro-apoptotic protein BIK is regulated by the ubiquitin-proteasome system. However, the mechanism of this regulation and its physiological functions remain elusive. Here, we identify Cul5-ASB11 as the E3 ligase targeting BIK for ubiquitination and degradation. ER stress leads to the activation of ASB11 by XBP1s during the adaptive phase of the unfolded protein response, which stimulates BIK ubiquitination, interaction with p97/VCP, and proteolysis. This mechanism of BIK degradation contributes to ER stress adaptation by promoting cell survival. Conversely, genotoxic agents down-regulate this IRE1α-XBP1s-ASB11 axis and stabilize BIK, which contributes in part to the apoptotic response to DNA damage. We show that blockade of this BIK degradation pathway by an IRE1α inhibitor can stabilize a BIK active mutant and increase its anti-tumor activity. Our study reveals that different cellular stresses regulate BIK ubiquitination by ASB11 in opposing directions, which determines whether or not cells survive, and that blocking BIK degradation has the potential to be used as an anti-cancer strategy.
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Registered trials
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