ArticleCurrent biology : CB2008
Aven-dependent activation of ATM following DNA damage.
Article in Current biology : CB, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- A multiomics Mendelian randomization study on PANoptosis-related genes and gastric cancer risk.The Journal of international medical research · 2026Article
- Prognostic and immunological potential of AC012236.1/hsa-miR-30d-5p CeRNA of AVEN by integrated analysis of single-cell and bulk RNA-seq in lung adenocarcinoma.Scientific reports · 2025Article
- Integrative proteomics and m6A microarray analyses of the signatures induced by METTL3 reveals prognostically significant in gastric cancer by affecting cellular metabolism.Frontiers in oncology · 2022Article
- Article
- Mammalian RNA Decay Pathways Are Highly Specialized and Widely Linked to Translation.Molecular cell · 2020Article
- The Viral Bcl-2 Homologs of Kaposi's Sarcoma-Associated Herpesvirus and Rhesus Rhadinovirus Share an Essential Role for Viral Replication.Journal of virology · 2017Article
- DNA damage response in cisplatin-induced nephrotoxicity.Archives of toxicology · 2015Review
- Aven recognition of RNA G-quadruplexes regulates translation of the mixed lineage leukemia protooncogenes.eLife · 2015Article
- Viral Bcl-2 Encoded by the Kaposi's Sarcoma-Associated Herpesvirus Is Vital for Virus Reactivation.Journal of virology · 2015Article
- Aven is dynamically regulated during Xenopus oocyte maturation and is required for oocyte survival.Cell death & disease · 2013Article
- Oxaliplatin induces different cellular and molecular chemoresistance patterns in colorectal cancer cell lines of identical origins.BMC genomics · 2013Article
- Overexpression of the anti-apoptotic protein AVEN contributes to increased malignancy in hematopoietic neoplasms.Oncogene · 2013Article
- The ATM protein kinase: regulating the cellular response to genotoxic stress, and more.Nature reviews. Molecular cell biology · 2013Review
- Multiple functions of BCL-2 family proteins.Cold Spring Harbor perspectives in biology · 2013Review
- The Apaf-1-binding protein Aven is cleaved by Cathepsin D to unleash its anti-apoptotic potential.Cell death and differentiation · 2012Article
- An Integrated Bioinformatics and Computational Biology Approach Identifies New BH3-Only Protein Candidates.The open biology journal · 2012Article
- BID binds to replication protein A and stimulates ATR function following replicative stress.Molecular and cellular biology · 2011Article
- ATM protein kinase: the linchpin of cellular defenses to stress.Cellular and molecular life sciences : CMLS · 2011Review
- Flying to a halt: Drosophila Aven arrests the cell cycle.Cell cycle (Georgetown, Tex.) · 2011Article
- Identification of dAven, a Drosophila melanogaster ortholog of the cell cycle regulator Aven.Cell cycle (Georgetown, Tex.) · 2011Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundIn response to DNA damage, cells undergo either cell-cycle arrest or apoptosis, depending on the extent of damage and the cell's capacity for DNA repair. Cell-cycle arrest induced by double-stranded DNA breaks depends on activation of the ataxia-telangiectasia (ATM) protein kinase, which phosphorylates cell-cycle effectors such as Chk2 and p53 to inhibit cell-cycle progression. ATM is recruited to double-stranded DNA breaks by a complex of sensor proteins, including Mre11/Rad50/Nbs1, resulting in autophosphorylation, monomerization, and activation of ATM kinase.
resultsIn characterizing Aven protein, a previously reported apoptotic inhibitor, we have found that Aven can function as an ATM activator to inhibit G2/M progression. Aven bound to ATM and Aven overexpressed in cycling Xenopus egg extracts prevented mitotic entry and induced phosphorylation of ATM and its substrates. Immunodepletion of endogenous Aven allowed mitotic entry even in the presence of damaged DNA, and RNAi-mediated knockdown of Aven in human cells prevented autophosphorylation of ATM at an activating site (S1981) in response to DNA damage. Interestingly, Aven is also a substrate of the ATM kinase. Mutation of ATM-mediated phosphorylation sites on Aven reduced its ability to activate ATM, suggesting that Aven activation of ATM after DNA damage is enhanced by ATM-mediated Aven phosphorylation.
conclusionsThese results identify Aven as a new ATM activator and describe a positive feedback loop operating between Aven and ATM. In aggregate, these findings place Aven, a known apoptotic inhibitor, as a critical transducer of the DNA-damage signal.
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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.