Fas Ligand Protein

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  Subject Areas on Research

  • Acute pancreatitis induces FasL gene expression and apoptosis in the liver. 
  • Analysis of FasL and TRAIL induced apoptosis pathways in glioma cells. 
  • Apoptosis and B cell tolerance. 
  • Apoptotic variants as predictors of risk of oropharyngeal cancer recurrence after definitive radiotherapy. 
  • Camptothecin and Fas receptor agonists synergistically induce medulloblastoma cell death: ROS-dependent mechanisms. 
  • Chronic activation of the kinase IKKβ impairs T cell function and survival. 
  • Down-regulation of the orphan nuclear receptor ROR gamma t is essential for T lymphocyte maturation. 
  • Endogenous expression of transforming growth factor beta1 inhibits growth and tumorigenicity and enhances Fas-mediated apoptosis in a murine high-grade glioma model. 
  • Ex vivo pediatric brain tumors express Fas (CD95) and FasL (CD95L) and are resistant to apoptosis induction. 
  • Expansion or elimination of B cells in vivo: dual roles for CD40- and Fas (CD95)-ligands modulated by the B cell antigen receptor. 
  • FAS and FASLG genetic variants and risk for second primary malignancy in patients with squamous cell carcinoma of the head and neck. 
  • Fas on renal parenchymal cells does not promote autoimmune nephritis in MRL mice. 
  • Fas/FasL play a central role in pancreatitis-induced hepatocyte apoptosis. 
  • Functional polymorphisms in the promoter regions of the FAS and FAS ligand genes and risk of bladder cancer in south China: a case-control analysis. 
  • Hepatic allograft-derived Kupffer cells regulate T cell response in rats. 
  • Induction of plasma (TRAIL), TNFR-2, Fas ligand, and plasma microparticles after human immunodeficiency virus type 1 (HIV-1) transmission: implications for HIV-1 vaccine design. 
  • Kupffer cell-derived Fas ligand plays a role in liver injury and hepatocyte death. 
  • Loss of the perforin cytotoxic pathway predisposes mice to experimental cytomegalovirus retinitis. 
  • Metastatic colorectal cancer cells from patients previously treated with chemotherapy are sensitive to T-cell killing mediated by CEA/CD3-bispecific T-cell-engaging BiTE antibody. 
  • Nuclear factor-kappaB mediates Kupffer cell apoptosis through transcriptional activation of Fas/FasL. 
  • Phenotypic and functional characterization of cytotoxic T lymphocytes by flow cytometry. 
  • Polymorphisms of FAS and FAS ligand genes involved in the death pathway and risk and progression of squamous cell carcinoma of the head and neck. 
  • Polymorphisms of the FAS and FAS ligand genes associated with risk of cutaneous malignant melanoma. 
  • RORgamma t, a novel isoform of an orphan receptor, negatively regulates Fas ligand expression and IL-2 production in T cells. 
  • Repression of B7.2 on self-reactive B cells is essential to prevent proliferation and allow Fas-mediated deletion by CD4(+) T cells. 
  • Role of LAT in the granule-mediated cytotoxicity of CD8 T cells. 
  • Site disparities in apoptotic variants as predictors of risk for second primary malignancy in patients with squamous cell carcinoma of the head and neck. 
  • Soluble Fas ligand blocks destructive corneal inflammation in mouse models of corneal epithelial debridement and LPS induced keratitis. 
  • Subtype-Specific Radiation Response and Therapeutic Effect of FAS Death Receptor Modulation in Human Breast Cancer. 
  • The cytolytic molecules Fas ligand and TRAIL are required for murine thymic graft-versus-host disease. 
  • The oncogenic microRNA miR-21 promotes regulated necrosis in mice. 
  • The p35 relative, p49, inhibits mammalian and Drosophila caspases including DRONC and protects against apoptosis. 
  • The role of p65 NF-kappaB/RelA in pancreatitis-induced Kupffer cell apoptosis. 
  • Transgenic expression of the viral FLIP MC159 causes lpr/gld-like lymphoproliferation and autoimmunity. 
  • c-FLIP maintains tissue homeostasis by preventing apoptosis and programmed necrosis. 
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  Keywords of People

  • Ferrari, Guido, Professor in Surgery, Molecular Genetics and Microbiology
  • Weinhold, Kent James, Joseph W. and Dorothy W. Beard Distinguished Professor of Experimental Surgery, in the School of Medicine, Immunology