ArticleThe Journal of cell biology1998
E1B 19K inhibits Fas-mediated apoptosis through FADD-dependent sequestration of FLICE.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 106 citations in OpenAlex.
- A Dual Role for FADD in Human Precursor T-Cell Neoplasms.International journal of molecular sciences · 2022Article
- A motif within the armadillo repeat of Parkinson's-linked LRRK2 interacts with FADD to hijack the extrinsic death pathway.Scientific reports · 2018Article
- Prevention of apoptosis by the interaction between FIH1 and Bax.Molecular and cellular biochemistry · 2011Article
- Article
- Role of the polarity determinant crumbs in suppressing mammalian epithelial tumor progression.Cancer research · 2008Article
- Article
- Regulatory molecules involved in inflammasome formation with special reference to a key mediator protein, ASC.Seminars in immunopathology · 2007Review
- Caspase-8 prevents sustained activation of NF-kappaB in monocytes undergoing macrophagic differentiation.Blood · 2007Article
- FLASH links the CD95 signaling pathway to the cell nucleus and nuclear bodies.The EMBO journal · 2007Article
- The role of receptor internalization in CD95 signaling.The EMBO journal · 2006Article
- IL-4 and IL-10 inhibition of spontaneous monocyte apoptosis is associated with Flip upregulation.Inflammation · 2004Article
- Complex and dynamic redistribution of NF-kappaB signaling intermediates in response to T cell receptor stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cells.Genes & development · 2003Article
- A novel domain in adenovirus L4-100K is required for stable binding and efficient inhibition of human granzyme B: possible interaction with a species-specific exosite.Molecular and cellular biology · 2003Article
- Fas-associated death domain protein interacts with methyl-CpG binding domain protein 4: a potential link between genome surveillance and apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Bfl-1S, a novel alternative splice variant of Bfl-1, localizes in the nucleus via its C-terminus and prevents cell death.Oncogene · 2003Article
- E1A sensitizes cells to tumor necrosis factor alpha by downregulating c-FLIP S.Journal of virology · 2003Article
- Bak and Bax function to limit adenovirus replication through apoptosis induction.Journal of virology · 2002Article
- Regulation of the mitochondrial checkpoint in p53-mediated apoptosis confers resistance to cell death.Oncogene · 2002Article
- Binding of FADD and caspase-8 to molluscum contagiosum virus MC159 v-FLIP is not sufficient for its antiapoptotic function.Journal of virology · 2002Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
E1B 19K, the adenovirus Bcl-2 homologue, is a potent inhibitor of apoptosis induced by various stimuli including Fas and tumor necrosis factor-alpha. Fas and TNFR-1 belong to a family of cytokine-activated receptors that share key components in their signaling pathways, Fas-associating protein with death domain (FADD) and FADD-like interleukin-1beta-converting enzyme (FLICE), to induce an apoptotic response. We demonstrate here that E1B 19K and Bcl-xL are able to inhibit apoptosis induced by FADD, but not FLICE. Surprisingly, apoptosis was abrogated by E1B 19K and Bcl-xL when FADD and FLICE were coexpressed. Immunofluorescence studies demonstrated that FADD expression produced large insoluble death effector filaments that may represent oligomerized FADD. E1B 19K expression disrupted FADD filament formation causing FADD and FLICE to relocalize to membrane and cytoskeletal structures where E1B 19K is normally localized. E1B 19K, however, does not detectably bind to FADD, nor does it inhibit FADD and FLICE from being recruited to the death-inducing signaling complex (DISC) when Fas is stimulated. Thus, E1B 19K may inhibit Fas-mediated cell death downstream of FADD recruitment of FLICE but upstream of FLICE activation by disrupting FADD oligomerization and sequestering an essential component of the DISC.
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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.