ReviewResults and problems in cell differentiation2009
Many checkpoints on the road to cell death: regulation of Fas-FasL interactions and Fas signaling in peripheral immune responses.
Review in Results and problems in cell differentiation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 50 citations in OpenAlex.
- A New Function of the S100-A4 Protein (Mts1): Mts1 Stimulates the Activation of Cytotoxic Lymphocytes via the TREM-1 Receptor.International journal of molecular sciences · 2026Article
- Review
- Polymorphisms Influence the Expression of the Fas and FasL Genes in COVID-19.International journal of molecular sciences · 2025Article
- Therapeutics Potential of Cronassial in Experimental Autoimmune Encephalomyelitis: Insights Into Glycosphingolipids and Humoral Immunity.TheScientificWorldJournal · 2025Article
- AcetylatedFrontiers in oncology · 2025Article
- Rigid crosslinking of the CD3 complex leads to superior T cell stimulation.Frontiers in immunology · 2024Article
- Article
- Beyond GWAS-Could Genetic Differentiation within the Allograft Rejection Pathway Shape Natural Immunity to COVID-19?International journal of molecular sciences · 2022Article
- We refuse to die - T cells causing havoc.Biomedical journal · 2021Article
- Review
- Major Molecular Signaling Pathways in Oral Cancer Associated With Therapeutic Resistance.Frontiers in oral health · 2020Review
- Review
- HBV and HIV/HBV Infected Patients Have Distinct Immune Exhaustion and Apoptotic Serum Biomarker Profiles.Pathogens & immunity · 2019Article
- Hepatitis B Spliced Protein (HBSP) Suppresses Fas-Mediated Hepatocyte Apoptosis via Activation of PI3K/Akt Signaling.Journal of virology · 2018Article
- Cell polarity and adherens junction formation inhibit epithelial Fas cell death receptor signaling.The Journal of cell biology · 2018Article
- Positive effect of RORγt on the prognosis of thyroid papillary carcinoma patients combined with Hashimoto's thyroiditis.American journal of translational research · 2018Article
- MicroRNA-25 Negatively Regulates Cerebral Ischemia/Reperfusion Injury-Induced Cell Apoptosis Through Fas/FasL Pathway.Journal of molecular neuroscience : MN · 2016Article
- Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease.Journal of clinical & cellular immunology · 2016Article
- Structural Characterizations of the Fas Receptor and the Fas-Associated Protein with Death Domain Interactions.The protein journal · 2016Article
- Adrenal-Derived Hormones Differentially Modulate Intestinal Immunity in Experimental Colitis.Mediators of inflammation · 2016Article
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
Abstract
Interactions between the TNF-family receptor Fas (CD95) and Fas Ligand (FasL, CD178) can efficiently induce apoptosis and are critical for the maintenance of immunological self-tolerance. FasL is kept under strict control by transcriptional and posttranslational regulation. Surface FasL can be cleaved by metalloproteases, resulting in shed extracellular domains, and FasL can also traffic to secretory lysosomes. Each form of FasL has distinct biological functions. Fas is more ubiquitously expressed, but its apoptosis-inducing function is regulated by a number of mechanisms including submembrane localization, efficiency of receptor signaling complex assembly and activation, and bcl-2 family members in some circumstances. When apoptosis is not induced, Fas-FasL interactions can also trigger a number of activating and proinflammatory signals. Harnessing the apoptosis-inducing potential of Fas for therapy of cancer and autoimmune disease has been actively pursued, and despite a number of unexpected side-effects that result from manipulating Fas-FasL interactions, this remains a worthy goal.
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.