ArticleGenes & development2003
DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cells.
Article in Genes & development, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.
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Who cites it
159 citing papers in PubMed, 310 citations in OpenAlex.
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- Fibrillarin: bridging ribosome biogenesis and apoptosis in cellular stress and disease.Apoptosis : an international journal on programmed cell death · 2026Review
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- An oncolytic HAdV-5 with reduced surface charge combines diminished toxicity and improved tumor targeting.Molecular therapy. Oncology · 2024Article
- Mcl-1 Protein and Viral Infections: A Narrative Review.International journal of molecular sciences · 2024Review
- Apoptosis, autophagy, and cancer: the critical roleGenes & development · 2023Article
- Let's not take DNA breaks for granted. The importance of direct detection of DNA breaks for the successful development of DDR inhibitors.Frontiers in cell and developmental biology · 2023Review
- Differential responses of COPD macrophages to respiratory bacterial pathogens.ERJ open research · 2022Article
- Isoliensinine induces cervical cancer cell cycle arrest and apoptosis by inhibiting the AKT/GSK3α pathway.Oncology letters · 2022Article
- Interplay between protein acetylation and ubiquitination controls MCL1 protein stability.Cell reports · 2021Article
- Synergistic effect of chidamide and venetoclax on apoptosis in acute myeloid leukemia cells and its mechanism.Annals of translational medicine · 2021Article
- Chromosome alignment-maintaining phosphoprotein CHAMP1 plays a role in cell survival through regulating Mcl-1 expression.Cancer science · 2021Article
- The genotoxicity potential of luteolin is enhanced by CYP1A1 and CYP1A2 in human lymphoblastoid TK6 cells.Toxicology letters · 2021Article
- Antiapoptotic Bcl-2 family proteins BCL-xL and MCL-1 integrate neural progenitor survival and proliferation during postnatal cerebellar neurogenesis.Cell death and differentiation · 2021Article
- Ruxolitinib induces apoptosis of human colorectal cancer cells by downregulating the JAK1/2-STAT1-Mcl-1 axis.Oncology letters · 2021Article
- Animal Coronaviruses Induced Apoptosis.Life (Basel, Switzerland) · 2021Review
- Identification of the Bok Interactome Using Proximity Labeling.Frontiers in cell and developmental biology · 2021Article
- Oncolytic virotherapy promotes radiosensitivity in soft tissue sarcoma by suppressing anti-apoptotic MCL1 expression.PloS one · 2021Article
- MARCH5 requires MTCH2 to coordinate proteasomal turnover of the MCL1:NOXA complex.Cell death and differentiation · 2020Article
99 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Expression of adenovirus E1A deregulates cell proliferation to facilitate viral DNA replication, prompting the initiation of apoptosis signaled primarily through proapoptotic BAK in productively infected cells. We demonstrate here that in uninfected cells, BAK is complexed with the anti-apoptotic BCL-2 family member Myeloid Cell Leukemia 1 (MCL-1). E1A expression during infection resulted in the specific down-regulation of MCL-1 through destabilization of the protein and loss of the mRNA. Upon loss of the MCL-1-BAK complex, BAK complexed with either BAX in proapoptotic E1B mutant adenovirus-infected cells, or with the adenovirus BCL-2 homolog E1B 19K in cells infected with the wild-type virus in which apoptosis is inhibited. Loss of MCL-1 was required to initiate the apoptotic pathway in infected cells as restoration of MCL-1 expression rescued infected cells from E1A-induced apoptosis. Analogous to E1A expression, DNA damage down-regulates MCL-1, and adenovirus infection resulted in the accumulation of phosphorylated H2AX and ataxia-telangiectasia mutant protein (ATM), hallmarks of DNA double-strand breaks. Thus, MCL-1 may function by maintaining BAK in an inactive state, and the loss of MCL-1 upon activation of the DNA damage response, perhaps through replication stress induced in virus infected cells, may be required to initiate the apoptotic response.
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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.