ArticleCell death & disease2018
Inhibitor of apoptosis proteins are required for effective fusion of autophagosomes with lysosomes.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 31 citations in OpenAlex.
- VHL-Mediated SYT11 Degradation Suppresses Gastric Cancer Cell Growth and Invasion Through Downregulation of SPINK1.Journal of cellular and molecular medicine · 2025Article
- 6-thioguanine inhibits EV71 replication by reducing BIRC3-mediated autophagy.BMC microbiology · 2025Article
- Autophagy in Disease Onset and Progression.Aging and disease · 2024Review
- Review
- Intestinal Immune Imbalance is an Alarm in the Development of IBD.Mediators of inflammation · 2023Review
- SMAC Mimetic BV6 Co-Treatment Downregulates the Factors Involved in Resistance and Relapse of Cancer: IAPs and Autophagy.Biology · 2022Article
- Epstein Barr virus-mediated transformation of B cells from XIAP-deficient patients leads to increased expression of the tumor suppressor CADM1.Cell death & disease · 2022Article
- Increased migration and motility in XIAP-null cells mediated by the C-RAF protein kinase.Scientific reports · 2022Article
- Immune-mediated inflammatory diseases with chronic excess of serum interleukin-18.Frontiers in immunology · 2022Review
- Cell Survival and Cell Death at the Intersection of Autophagy and Apoptosis: Implications for Current and Future Cancer Therapeutics.ACS pharmacology & translational science · 2021Review
- Dysfunction of X-linked inhibitor of apoptosis protein (XIAP) triggers neuropathological processes via altered p53 activity in Huntington's disease.Progress in neurobiology · 2021Article
- XIAP Knockdown in Alcohol-Associated Liver Disease Models Exhibits DivergentFrontiers in physiology · 2021Article
- Evolution of Our Understanding of XIAP Deficiency.Frontiers in pediatrics · 2021Review
- Anti-apoptotic proteins in the autophagic world: an update on functions of XIAP, Survivin, and BRUCE.Journal of biomedical science · 2020Review
- New insights into the interplay between autophagy, gut microbiota and inflammatory responses in IBD.Autophagy · 2020Review
- Roles of ubiquitin in autophagy and cell death.Seminars in cell & developmental biology · 2019Review
- Supramolecular Complexes in Cell Death and Inflammation and Their Regulation by Autophagy.Frontiers in cell and developmental biology · 2019Review
- Recent advances in understanding inhibitor of apoptosis proteins.F1000Research · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibitor of Apoptosis Proteins act as E3 ubiquitin ligases to regulate NF-κB signalling from multiple pattern recognition receptors including NOD2, as well as TNF Receptor Superfamily members. Loss of XIAP in humans causes X-linked Lymphoproliferative disease type 2 (XLP-2) and is often associated with Crohn's disease. Crohn's disease is also caused by mutations in the gene encoding NOD2 but the mechanisms behind Crohn's disease development in XIAP and NOD2 deficient-patients are still unknown. Numerous other mutations causing Crohn's Disease occur in genes controlling various aspects of autophagy, suggesting a strong involvement of autophagy in preventing Crohn's disease. Here we show that the IAP proteins cIAP2 and XIAP are required for efficient fusion of lysosomes with autophagosomes. IAP inhibition or loss of both cIAP2 and XIAP resulted in a strong blockage in autophagic flux and mitophagy, suggesting that XIAP deficiency may also drive Crohn's Disease due to defects in autophagy.
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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.