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FASLG protein, human

FASLG (Fas Ligand) is a type II membrane protein that belongs to the tumor necrosis factor (TNF) superfamily.
It plays a crucial role in the regulation of programmed cell death (apoptosis) and is involved in various physiological and pathological processes.
FASLG binds to its receptor, Fas (CD95), which triggers a signaling cascade leading to caspase activation and cell death.
This protein is expressed in a variety of cell types, including activated T cells, natural killer cells, and some non-lymphoid cells.
Dysregulation of FASLG has been implicated in the pathogenesis of autoimmune diseases, cancer, and other disorders.
Understanding the biology and fuction of FASLG is essential for developing therapies targeting this important protein. [Note: There is a typo in the word 'function' in the previous sentence.]

Most cited protocols related to «FASLG protein, human»

1
Single-Cell Gene Expression Modeling
Cited 68 times
As described previously, for a given cell, a gene can be defined as on (i.e. a positive et value is recorded) or as off (i.e. the gene is undetected and ). To simplify our model, we will denote by the indicator variable equal to one if the gene is expressed in well and zero otherwise. Following classical statistical conventions, we use upper cases to denote the random variables and lower cases to denote the values taken by these random variables. Using these notations, we introduce the following model of single-cell expression



where denotes a point mass at zero, and are the -based mean and variance expression-level parameters conditional on the gene being expressed (i.e. ), and is the frequency of expression of gene across all cells. In the datasets considered here, the frequency of expression greatly varies across genes from 0 to 0.99 with a median value of ∼0.1 (see Supplementary Fig. S1). Assuming a log-Normal model for is equivalent to modeling as normally distributed. The empirical distribution of the data (Fig. 1 and Supplementary Figs S8–S10) motivates our selection of a log-normal distribution and follows observations of previous authors (Bengtsson et al., 2005 (link)).

Histogram and theoretical (normal) distribution of for single-cell (left, light gray) and 100-cell experiments (right, dark gray). Genes FASLG, IFN- , BIRC3 and CD69 are depicted. The frequency expression of each gene in the single-cell experiments is printed above each histogram. The mean of the 100-cell and single-cell experiments is indicated by a thick black line along the x-axis

Thus, in a particular gene, three parameters characterize the expression distribution: , the mean and standard deviation of the , and , the Bernoulli probability of expression.
McDavid A., Finak G., Chattopadyay P.K., Dominguez M., Lamoreaux L., Ma S.S., Roederer M, & Gottardo R. (2012). Data exploration, quality control and testing in single-cell qPCR-based gene expression experiments. Bioinformatics, 29(4), 461-467.
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Publication 2012
BIRC3 protein, human Cells Conferences FASLG protein, human Gene Expression Genes Light
2
Organotypic Brain Slice Culture for Cancer Study
Cited 15 times

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Publication 2014
Adult alpha 2-Plasmin Inhibitor Antibodies, Blocking Aves benzamide Bicarbonate, Sodium Brain Caspase 3 Cell Nucleus Cells Collagen Type IV FASLG protein, human Glucose Gold HEPES Immunofluorescence Innovativeness Malignant Neoplasms Mice, Nude Mus Penicillins Plasminogen Activator Inhibitor 2 Sepharose Sodium Chloride Streptomycin Sulfate, Magnesium Tissue, Membrane Tissues
3
Murine Tumor Models for Immunotherapy
Cited 12 times
Animals were housed and treated under an animal protocol approved by the institutional animal care and use committee. Female mice were purchased at age 6-8 weeks from Taconic (C57BL/6 and Fcγ receptor-deficient C57BL/6.129P2-Fcer1gtm1Rav N12), Harlan (NcR nude mice), and Jackson ( A/J and FasL deficient C57BL/6 Smn.C3-Tnfsf6gld/J).
B78, B16, NXS2, and Panc02 tumors were engrafted by subcutaneous flank injection of 2×106 tumor cells. For disseminated disease models 3.5×105 B16 cells were IV injected. Engraftment of SCC1-C was performed by subcutaneous flank injection of 3×106 cells = in 2:1 PBS:Matrigel (BD Biosciences).
Tumor size was determined using calipers and volume approximated as (width2 × length)/2. Mice were randomized immediately prior to treatment. The day of radiation was defined as “day 1” of treatment. IT injections were made by a single percutaneous needle puncture followed by injection of a 100 µL volume with needle redirection to distribute injected material around the tumor. IT injections of 50 µg hu14.18K322A, cetuximab, hu14.18-IL2, or control IgG were delivered daily on days 6-10. Anti-CTLA-4 or control IgG was administered by 200 µg intraperitoneal (IP) injection days 3, 6, and 9. For NK cell depletion, IP injections of 500 µg NK1.1 mAb (clone PK136, ATCC) were delivered days 1, 5, 10, and 15. Depletion of T cells was performed as previously described (22 (link)).
Treatment began when tumors were well established (~200 mm3), occurring ~ 5 weeks after tumor implantation for B78 melanoma. For “large” B78 tumors (~500 mm3), treatment began ~ 7 weeks after implantation. Animals were sacrificed when tumors exceeded a pre-determined dimension. Mouse experiments were repeated in triplicate. Final replicates are presented for tumor response and aggregate data for survival; number of animals (n) per group is indicated.
Morris Z.S., Guy E.I., Francis D.M., Gressett M.M., Werner L.R., Carmichael L.L., Yang R.K., Armstrong E.A., Huang S., Navid F., Gillies S.D., Korman A., Hank J.A., Rakhmilevich A.L., Harari P.M, & Sondel P.M. (2016). In situ tumor vaccination by combining local radiation and tumor-specific antibody or immunocytokine treatments. Cancer research, 76(13), 3929-3941.
Publication 2016
Animals Cells Cetuximab Clone Cells Cytotoxic T-Lymphocyte Antigen 4 FASLG protein, human hu14.18-IL2 Injections, Intraperitoneal Institutional Animal Care and Use Committees matrigel Melanoma Mice, Nude Mus Natural Killer Cells Needles Neoplasms Ovum Implantation Punctures Radiation Receptors, IgG Subcutaneous Injections T-Lymphocyte Woman
4
Reduced Discrete System Modeling
Cited 8 times
We have used a model reduction technique specifically adapted to discrete systems, which mainly consists in iteratively “hiding” some variables, while keeping track of underlying regulatory processes [47] . The main dynamical properties of the master model, including stable states and other attractors are conserved in the reduced model. Thanks to the computation of the reduced asynchronous transition graph, relevant qualitative dynamical properties of the model can be compared to experimental results for wild type and in different mutant cases.
To reduce the number of species in the master model, each logical rule is considered. For each removed component, the information contained in its rule is included in the rules of its targets such that no effective regulation is lost.
Many intermediate components could easily be replaced by a proper rewriting of the logical rules associated with their target nodes. For example, IKK has only one input (RIP1ub) and one output (NFκB). Since its role in our model merely consists in transmitting the signal from RIP1ub to NFκB, it can be easily replaced by a straightforward change in the logical rule associated with NFκB (implementing a direct activation from RIP1ub instead of IKK). We also relied on the results of the clustering of stable states and their associations with biologically plausible phenotypes to select the key components to keep in the reduced model: NFκB is the principal survival actor, while caspases-3 and -8, together with the mitochondrial membrane permeability variables (MOMP and MPT), determine apoptotic and non-apoptotic cell deaths.
Let us consider the example of the removal of BAX and BCL2 (Figure 1 A and B). The regulators (or inputs) of these variables are NFκB for BCL2 and CASP8 for BAX while their regulating targets (or outputs) are MPT for BCL2 and MOMP for BAX. BCL2 is directly activated by NFκB, and has two targets: MPT and BAX. Therefore, BCL2 removal is performed by replacing BCL2 by NFκB into the rules of the two targets, leading to the two new logical rules: MPT′ = ROS AND NOT NFkB and BAX′ = C8 AND NOT NFkB. Applying the same process to remove BAX, one obtains the following new rule for MOMP: MOMP′ = MPT OR (C8 AND NOT NFkB).
The variables MOMP and MPT have now as inputs the variables NFκB and CASP8. One can see that, in spite of the disappearance of variables BAX and BCL2, their regulating roles are still indirectly coded in the reduced system, ensuring that no “logical interaction” of the master model (i.e. activation or inhibition) is actually lost during the reduction process. Table S3 lists the variables of the master model that are removed to obtain the reduced model.
Some hypotheses were made when reducing the model. First, FADD is considered to be constantly ON in wild type simulations. Second, since the two complexes TNFR and DISC-TNF have been removed together with the input FADD, the two deaths ligands TNF and L have the exact same action in the reduced model. Indeed, we consider that, in response to FAS death receptor engagement as well as that of TNF; the activations of both the survival and necrotic pathways RIP1-dependent. In this case, one could then merge these variables and consider only one input that could be called “external death receptor”. However, we choose to keep the two variables TNF and FASL, in the FADD deletion mutant, the phenotype differs for TNF and FAS signal: actually, only for that mutant is the symmetry of TNF and FAS broken.
Calzone L., Tournier L., Fourquet S., Thieffry D., Zhivotovsky B., Barillot E, & Zinovyev A. (2010). Mathematical Modelling of Cell-Fate Decision in Response to Death Receptor Engagement. PLoS Computational Biology, 6(3), e1000702.
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Publication 2010
Apoptosis BCL2 protein, human CASP8 protein, human Caspase 3 CD95 Antigens Cell Membrane Permeability Deletion Mutation FADD protein, human FASLG protein, human Ligands Mitochondria Mitochondrial Membranes Necrosis Permeability Phenotype Psychological Inhibition Receptors, Death Domain RELA protein, human Tumor Necrosis Factor Receptor
5
Antibody Preparation and Handling
Cited 8 times
Anti–mouse CD16/32 (FcR) mAb (2.4G2), anti–mouse CD11b mAb (5C6), control hamster Ig (UC8-1B9), anti–mouse CD4 mAb (GK1.5), anti–mouse CD8 mAb (53-6.7), anti–mouse FasL mAb (MFL3), and anti–mouse TRAIL mAb (N2B2) were prepared in our laboratory as previously described (4 (link), 19 (link)). Biotinylated anti–mouse F4/80 mAb (A3-1) was purchased from Caltag, biotinylated anti–mouse CD205 mAb (NLDC-145) was purchased from Cedarlane Laboratories, and biotinylated rat IgG2aκ (R35-95) and rat IgG 2bκ (A95-1) were purchased from BD Biosciences. A hamster IgG2 anti–mouse DR5 mAb (MD5-1) was generated by immunizing an Armenian hamster with mouse DR5-Ig fusion protein (DakoCytomation), fusing the splenocytes with P3U1 mouse myeloma cells, and then screening the reactivity to mouse DR5-transfected BHK (BHK-mDR5) cells by flow cytometry. MD5-1 was purified from ascites using a protein G column. Biotinylation was performed as previously described (20 (link)). Requests for MD5-1 should be addressed to H. Yagita (hyagita@med.juntendo.ac.jp).
Takeda K., Yamaguchi N., Akiba H., Kojima Y., Hayakawa Y., Tanner J.E., Sayers T.J., Seki N., Okumura K., Yagita H, & Smyth M.J. (2004). Induction of Tumor-specific T Cell Immunity by Anti-DR5 Antibody Therapy. The Journal of Experimental Medicine, 199(4), 437-448.
Publication 2004
Ascites Biotinylation CD205 antigen Cells FASLG protein, human Flow Cytometry G-substrate Hamsters Hamsters, Armenian IgG2 ITGAM protein, human Multiple Myeloma Mus Proteins Staphylococcal Protein A TNFSF10 protein, human

Most recents protocols related to «FASLG protein, human»

1
Caspase-3 Activity Assay in Senescent Cells
The effect of SOC drugs on caspase-3 activity was observed by using Caspase-3/CPP32 Fluorometric Assay Kit (BioVision Inc). Senescent fibroblasts were treated with SOC drugs or D + Q for 24 h, followed by 3 h of Super FasL stimuli. Cells were lysed in 50 μl chilled cell lysis buffer on ice for 10 min before 50 μl of 2× reaction buffer (containing 10 mM Dithiothreitol) was added, followed by 50 μM DEVD-AFC substrate, incubated at 37 °C for 2 h. Fluorescence was measured at 505 nm with a fluorescent microplate reader (Biotek). Results were expressed as fold-change compared to control cells.
Badaro-Garcia S., Hohmann M.S., Coelho A.L., Verri WA J.r, & Hogaboam C.M. (2023). Standard of care drugs do not modulate activity of senescent primary human lung fibroblasts. Scientific Reports, 13, 3654.
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Publication 2023
aspartyl-glutamyl-valyl-aspartyl-7-amino-4-trifluoromethylcoumarin Biological Assay Buffers CASP3 protein, human Caspase 3 Cells Dithiothreitol FASLG protein, human Fibroblasts Fluorescence Fluorometry Pharmaceutical Preparations
2
Evaluating Senescent Lung Fibroblast Viability
Cell viability was evaluated using AlamarBlue Cell Viability Reagent (ThermoFisher Scientific). Senescent lung fibroblasts (3 × 104 cells/well) were treated with nintedanib (Ofev, Boehringer Ingelheim, Germany; 300 nM), pirfenidone (Esbriet, Genentech, San Francisco; 2.5 mM) or dasatinib (Tocris, Bristol, UK; 20 μM) + quercetin (Sigma-Aldrich, St. Louis, MO; 15 μM) for 24 h followed by 3 h with the cell death ligand Super Fas Ligand (100 ng/ml). AlamarBlue Cell Viability Reagent was added to the cells and incubated for 4 h at 37 °C. Fluorescence values were assessed using a fluorescence excitation wavelength of 560 nm and an emission of 590 nm with a fluorescent microplate reader (Biotek). Results were expressed as fold-change compared to control cells.
Badaro-Garcia S., Hohmann M.S., Coelho A.L., Verri WA J.r, & Hogaboam C.M. (2023). Standard of care drugs do not modulate activity of senescent primary human lung fibroblasts. Scientific Reports, 13, 3654.
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Publication 2023
Alamar Blue Cell Death Cells Cell Survival Dasatinib Esbriet FASLG protein, human Fibroblasts Fluorescence Ligands Lung nintedanib Ofev pirfenidone Quercetin
3
Isolation and Fractionation of Lignin

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Publication 2023
Acetone Acids Centrifugation FASLG protein, human Freezing Lignin Powder Pressure Solvents Vacuum Viscosity
4
Epoxidation of Lignin Fractions

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Publication 2023
Acetone Centrifugation Epichlorohydrin FASLG protein, human Freeze Drying Lignin Sodium Hydroxide
5
Isolation and Analysis of Intrahepatic Immune Cells
Intrahepatic mononuclear cells and mouse primary hepatocytes were isolated from the liver as described previously36 (link), washed, pelleted, and resuspended in staining buffer (Thermo Fisher Scientific, Waltham, MA) and stained with specific antibodies, as described.36 (link) Primary antibodies that were used targeted F4/80, CD178 and CD95 (Thermo Fisher Scientific, Waltham, MA). Flow-assisted cell analysis was conducted at the University of Colorado Cancer Center Flow Cytometry Core Facility and were performed on Yeti flow cytometry device (Bio-rad) and data were analyzed by Kaluza software (Beckman Coulter, Brea, CA).
Ghosh S., Devereaux M.W., Anderson A.L., El Kasmi *.C, & Sokol R.J. (2023). Stat3 role in the protective effect of FXR Agonist in parenteral nutrition-associated cholestasis. Hepatology Communications, 7(3), e0056.
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Publication 2023
Antibodies Buffers Cells FASLG protein, human Flow Cytometry Hepatocyte Liver Malignant Neoplasms Medical Devices Mus

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Lipofectamine 2000 is a cationic lipid-based transfection reagent designed for efficient and reliable delivery of nucleic acids, such as plasmid DNA and small interfering RNA (siRNA), into a wide range of eukaryotic cell types. It facilitates the formation of complexes between the nucleic acid and the lipid components, which can then be introduced into cells to enable gene expression or gene silencing studies.
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