ArticleOncogene2005
Oxidative stress attenuates Fas-mediated apoptosis in Jurkat T cell line through Bfl-1 induction.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 51 citations in OpenAlex.
- Catalase inhibition can modulate the ability of peripheral blood T cells to undergo apoptosis in Crohn's disease.Clinical and experimental immunology · 2024Article
- Key pathways and genes that are altered during treatment with hyperbaric oxygen in patients with sepsis due to necrotizing soft tissue infection (HBOmic study).European journal of medical research · 2023Observational
- BCL2A1 regulates Canady Helios Cold Plasma-induced cell death in triple-negative breast cancer.Scientific reports · 2022Article
- CDCA2 protects against oxidative stress by promoting BRCA1-NRF2 signaling in hepatocellular carcinoma.Oncogene · 2021Article
- Precision Targeting of BFL-1/A1 and an ATM Co-dependency in Human Cancer.Cell reports · 2018Article
- Possible Biomarkers in Blood for Crohn's Disease: Oxidative Stress and MicroRNAs-Current Evidences and Further Aspects to Unravel.Oxidative medicine and cellular longevity · 2016Review
- Decitabine induces delayed reactive oxygen species (ROS) accumulation in leukemia cells and induces the expression of ROS generating enzymes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- BCL2A1: the underdog in the BCL2 family.Cell death and differentiation · 2012Review
- Cancer cell survival following DNA damage-mediated premature senescence is regulated by mammalian target of rapamycin (mTOR)-dependent Inhibition of sirtuin 1.The Journal of biological chemistry · 2011Article
- Article
- A global transcriptional view of apoptosis in human T-cell activation.BMC medical genomics · 2008Article
- Common and distinct mechanisms of different redox-active carcinogens involved in the transformation of mouse JB6P+ cells.Molecular carcinogenesis · 2008Article
- Nur77 upregulates HIF-alpha by inhibiting pVHL-mediated degradation.Experimental & molecular medicine · 2008Article
- Glutathione depletion is necessary for apoptosis in lymphoid cells independent of reactive oxygen species formation.The Journal of biological chemistry · 2007Article
- Potential targets of FOXL2, a transcription factor involved in craniofacial and follicular development, identified by transcriptomics.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many types of mammalian cells produce ROS in response to many different stimuli to modulate a number of cellular functions, including apoptosis. However, the correlation between ROS and apoptosis remains controversial, and the mechanisms whereby ROS-induced signals are propagated to critical downstream targets remain largely undefined. Here, we demonstrate that hydrogen peroxide (H2O2) upregulates the expression of Bfl-1, an antiapoptotic member of the Bcl-2 family, and that this is responsible for the antiapoptotic activity of ROS. When Jurkat, human leukemic T cells, were pretreated with 100 microM H2O2 and then treated with anti-Fas antibody, apoptosis was impaired without change of cell surface Fas expression. An investigation of the expression patterns of Bcl-2 family genes revealed that H2O2 treatment induced Bfl-1 gene expression, but left other genes unchanged, and this Bfl-1 expression and H2O2 -induced antiapoptotic effect was inhibited by antioxidants or NF-kappaB inhibitor. In addition, an electromobility shift assay revealed that the p65/p50 subunits of NF-kappaB activated by H2O2 bound to a bfl-1 promoter. Neither the induction of Bfl-1 nor the antiapoptotic effect of H2O2 was detected in Bfl-1-knockdown Jurkat cell line containing Bfl-1 antisense (Bfl-1AS). These data indicate that oxidative stress induces the expression of Bfl-1 via NF-kappaB activation, and this early-response gene protects cells from Fas-mediated apoptosis. This may be a cellular survival mechanism of cells exposed to phagocytes-derived ROS.
Indexed as
Identifiers
What OpenQuestion holds
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.