ArticleOncogene2003
The early response gene IEX-1 attenuates NF-kappaB activation in 293 cells, a possible counter-regulatory process leading to enhanced cell death.
Article in Oncogene, 2003. 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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Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- YTHDF2-mediated mFrontiers in cellular and infection microbiology · 2025Article
- STAT3 regulates inflammatory cytokine production downstream of TNFR1 by inducing expression of TNFAIP3/A20.Journal of cellular and molecular medicine · 2022Article
- Inhibitory feedback control of NF-κB signalling in health and disease.The Biochemical journal · 2021Review
- Emerging Potential of Immediate Early Response Gene X-1 in Cardiovascular and Metabolic Diseases.Journal of the American Heart Association · 2018Article
- Exome and transcriptome sequencing identifies loss ofCancer management and research · 2017Article
- The RNA-binding protein TTP is a global post-transcriptional regulator of feedback control in inflammation.Nucleic acids research · 2016Article
- P2X7 receptor activation regulates rapid unconventional export of transglutaminase-2.Journal of cell science · 2015Article
- IER3 is a crucial mediator of TAp73β-induced apoptosis in cervical cancer and confers etoposide sensitivity.Scientific reports · 2015Article
- Transcriptomic and Functional Pathway Analysis of Human Cervical Carcinoma Cancer Cells Response to Microtubule Inhibitor.Journal of Cancer · 2015Article
- IER3 supports KRASG12D-dependent pancreatic cancer development by sustaining ERK1/2 phosphorylation.The Journal of clinical investigation · 2014Article
- Modulation of nuclear factor E2-related factor-2 (Nrf2) activation by the stress response gene immediate early response-3 (IER3) in colonic epithelial cells: a novel mechanism of cellular adaption to inflammatory stress.The Journal of biological chemistry · 2014Article
- Ablation of gly96/immediate early gene-X1 (gly96/iex-1) aggravates DSS-induced colitis in mice: role for gly96/iex-1 in the regulation of NF-kappaB.Inflammatory bowel diseases · 2010Article
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- Immediate early gene-X1 interferes with 26 S proteasome activity by attenuating expression of the 19 S proteasomal components S5a/Rpn10 and S1/Rpn2.The Biochemical journal · 2007Article
- Array-based comparative gene expression analysis of tumor cells with increased apoptosis resistance after hypoxic selection.Oncogene · 2005Article
- Immediate early gene X-1 interacts with proteins that modulate apoptosis.Biochemical and biophysical research communications · 2004Article
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Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The early response gene IEX-1 is involved in the regulation of cellular growth and survival, and its expression is related to stress-, growth- and death-inducing signals. Addressing the role of IEX-1 in the promotion of apoptosis, we investigated the effect of IEX-1 on nuclear factor-kappaB (NF-kappaB) activation. Stably transfected HEK-293 cells conditionally overexpressing IEX-1 exhibit decreased levels of NF-kappaB activity, either basal or TNFalpha induced, as shown by gel-shift and luciferase reporter gene assay. Furthermore, activated p65 accumulated in the nuclei of 293 cells to a lower degree, if IEX-1 expression was increased. This inhibited NF-kappaB activation was preceded by an altered turnover of IkappaBalpha and phospho-IkappaBalpha. In addition, IEX-1 expression also inhibited the activity of the 26S-proteasome, as shown by a fluorometric proteasome assay. Conversely, disruption of IEX-1 expression in 293 cells by stable transfection with specific anti-IEX-1 hammerhead ribozymes increased NF-kappaB activity, and accelerated the degradation of IkappaBalpha. Along with these opposite effects of IEX-1 expression and IEX-1 disruption on NF-kappaB activation, the sensitivity of 293 cells towards various apoptotic stimuli also changed. In contrast to ribozyme-transduced 293 cells that were significantly less sensitive to apoptosis, this sensitivity was enhanced if IEX-1 expression was increased. Our data suggest that IEX-1 - itself an NF-kappaB target gene - inhibits the activation of this transcription factor, and hereby may counteract the antiapoptotic potential of NF-kappaB.
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