Browse FAS

Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Basic function annotation.
> Subcellular Location, Domain and Function
> Gene Ontology
> KEGG and Reactome Pathway
> Subcellular Location, Domain and Function
 
Subcellular Location Isoform 1: Cell membrane; Single-pass type I membrane protein.; SUBCELLULAR LOCATION: Isoform 2: Secreted.; SUBCELLULAR LOCATION: Isoform 3: Secreted.; SUBCELLULAR LOCATION: Isoform 4: Secreted.; SUBCELLULAR LOCATION: Isoform 5: Secreted.; SUBCELLULAR LOCATION: Isoform 6: Secreted.
Domain PF00531 Death domain
PF00020 TNFR/NGFR cysteine-rich region
Function

Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. The secreted isoforms 2 to 6 block apoptosis (in vitro).

> Gene Ontology
 
Biological Process GO:0001776 leukocyte homeostasis
GO:0002237 response to molecule of bacterial origin
GO:0002250 adaptive immune response
GO:0002260 lymphocyte homeostasis
GO:0002377 immunoglobulin production
GO:0002440 production of molecular mediator of immune response
GO:0002443 leukocyte mediated immunity
GO:0002449 lymphocyte mediated immunity
GO:0002460 adaptive immune response based on somatic recombination of immune receptors built from immunoglobulin superfamily domains
GO:0002521 leukocyte differentiation
GO:0002683 negative regulation of immune system process
GO:0002694 regulation of leukocyte activation
GO:0002695 negative regulation of leukocyte activation
GO:0003014 renal system process
GO:0006919 activation of cysteine-type endopeptidase activity involved in apoptotic process
GO:0006924 activation-induced cell death of T cells
GO:0006925 inflammatory cell apoptotic process
GO:0007159 leukocyte cell-cell adhesion
GO:0007623 circadian rhythm
GO:0008625 extrinsic apoptotic signaling pathway via death domain receptors
GO:0009612 response to mechanical stimulus
GO:0009636 response to toxic substance
GO:0010035 response to inorganic substance
GO:0010038 response to metal ion
GO:0010226 response to lithium ion
GO:0010950 positive regulation of endopeptidase activity
GO:0010952 positive regulation of peptidase activity
GO:0019724 B cell mediated immunity
GO:0030098 lymphocyte differentiation
GO:0030099 myeloid cell differentiation
GO:0030217 T cell differentiation
GO:0031334 positive regulation of protein complex assembly
GO:0031960 response to corticosteroid
GO:0032459 regulation of protein oligomerization
GO:0032461 positive regulation of protein oligomerization
GO:0032462 regulation of protein homooligomerization
GO:0032464 positive regulation of protein homooligomerization
GO:0032496 response to lipopolysaccharide
GO:0033077 T cell differentiation in thymus
GO:0033209 tumor necrosis factor-mediated signaling pathway
GO:0034612 response to tumor necrosis factor
GO:0036295 cellular response to increased oxygen levels
GO:0036296 response to increased oxygen levels
GO:0038034 signal transduction in absence of ligand
GO:0042110 T cell activation
GO:0042113 B cell activation
GO:0043029 T cell homeostasis
GO:0043254 regulation of protein complex assembly
GO:0043280 positive regulation of cysteine-type endopeptidase activity involved in apoptotic process
GO:0043281 regulation of cysteine-type endopeptidase activity involved in apoptotic process
GO:0043383 negative T cell selection
GO:0043410 positive regulation of MAPK cascade
GO:0044089 positive regulation of cellular component biogenesis
GO:0045058 T cell selection
GO:0045060 negative thymic T cell selection
GO:0045061 thymic T cell selection
GO:0045619 regulation of lymphocyte differentiation
GO:0045637 regulation of myeloid cell differentiation
GO:0045862 positive regulation of proteolysis
GO:0048511 rhythmic process
GO:0048536 spleen development
GO:0048545 response to steroid hormone
GO:0048872 homeostasis of number of cells
GO:0050864 regulation of B cell activation
GO:0050865 regulation of cell activation
GO:0050866 negative regulation of cell activation
GO:0050869 negative regulation of B cell activation
GO:0051249 regulation of lymphocyte activation
GO:0051250 negative regulation of lymphocyte activation
GO:0051259 protein oligomerization
GO:0051260 protein homooligomerization
GO:0051384 response to glucocorticoid
GO:0051402 neuron apoptotic process
GO:0052547 regulation of peptidase activity
GO:0052548 regulation of endopeptidase activity
GO:0055093 response to hyperoxia
GO:0070227 lymphocyte apoptotic process
GO:0070228 regulation of lymphocyte apoptotic process
GO:0070230 positive regulation of lymphocyte apoptotic process
GO:0070231 T cell apoptotic process
GO:0070265 necrotic cell death
GO:0070266 necroptotic process
GO:0070482 response to oxygen levels
GO:0070486 leukocyte aggregation
GO:0070489 T cell aggregation
GO:0070997 neuron death
GO:0071214 cellular response to abiotic stimulus
GO:0071241 cellular response to inorganic substance
GO:0071248 cellular response to metal ion
GO:0071260 cellular response to mechanical stimulus
GO:0071285 cellular response to lithium ion
GO:0071356 cellular response to tumor necrosis factor
GO:0071453 cellular response to oxygen levels
GO:0071455 cellular response to hyperoxia
GO:0071496 cellular response to external stimulus
GO:0071593 lymphocyte aggregation
GO:0071594 thymocyte aggregation
GO:0071887 leukocyte apoptotic process
GO:0097049 motor neuron apoptotic process
GO:0097191 extrinsic apoptotic signaling pathway
GO:0097192 extrinsic apoptotic signaling pathway in absence of ligand
GO:0097284 hepatocyte apoptotic process
GO:0097296 activation of cysteine-type endopeptidase activity involved in apoptotic signaling pathway
GO:0097300 programmed necrotic cell death
GO:0097527 necroptotic signaling pathway
GO:1902041 regulation of extrinsic apoptotic signaling pathway via death domain receptors
GO:1902042 negative regulation of extrinsic apoptotic signaling pathway via death domain receptors
GO:1902105 regulation of leukocyte differentiation
GO:1903706 regulation of hemopoiesis
GO:1904019 epithelial cell apoptotic process
GO:2000106 regulation of leukocyte apoptotic process
GO:2000108 positive regulation of leukocyte apoptotic process
GO:2000116 regulation of cysteine-type endopeptidase activity
GO:2001056 positive regulation of cysteine-type endopeptidase activity
GO:2001233 regulation of apoptotic signaling pathway
GO:2001234 negative regulation of apoptotic signaling pathway
GO:2001235 positive regulation of apoptotic signaling pathway
GO:2001236 regulation of extrinsic apoptotic signaling pathway
GO:2001237 negative regulation of extrinsic apoptotic signaling pathway
GO:2001238 positive regulation of extrinsic apoptotic signaling pathway
GO:2001239 regulation of extrinsic apoptotic signaling pathway in absence of ligand
GO:2001241 positive regulation of extrinsic apoptotic signaling pathway in absence of ligand
GO:2001267 regulation of cysteine-type endopeptidase activity involved in apoptotic signaling pathway
GO:2001269 positive regulation of cysteine-type endopeptidase activity involved in apoptotic signaling pathway
Molecular Function GO:0005031 tumor necrosis factor-activated receptor activity
GO:0005035 death receptor activity
Cellular Component GO:0009897 external side of plasma membrane
GO:0031264 death-inducing signaling complex
GO:0031265 CD95 death-inducing signaling complex
GO:0045121 membrane raft
GO:0098552 side of membrane
GO:0098589 membrane region
GO:0098857 membrane microdomain
> KEGG and Reactome Pathway
 
KEGG hsa04010 MAPK signaling pathway
hsa04060 Cytokine-cytokine receptor interaction
hsa04115 p53 signaling pathway
hsa04210 Apoptosis
hsa04650 Natural killer cell mediated cytotoxicity
hsa04668 TNF signaling pathway
Reactome R-HSA-109581: Apoptosis
R-HSA-5218900: CASP8 activity is inhibited
R-HSA-5357769: Caspase activation via extrinsic apoptotic signalling pathway
R-HSA-73887: Death Receptor Signalling
R-HSA-69416: Dimerization of procaspase-8
R-HSA-75157: FasL/ CD95L signaling
R-HSA-74160: Gene Expression
R-HSA-212436: Generic Transcription Pathway
R-HSA-140534: Ligand-dependent caspase activation
R-HSA-5357801: Programmed Cell Death
R-HSA-5213460: RIPK1-mediated regulated necrosis
R-HSA-5218859: Regulated Necrosis
R-HSA-3371378: Regulation by c-FLIP
R-HSA-5675482: Regulation of necroptotic cell death
R-HSA-162582: Signal Transduction
R-HSA-5633008: TP53 Regulates Transcription of Cell Death Genes
R-HSA-6803211: TP53 Regulates Transcription of Death Receptors and Ligands
R-HSA-3700989: Transcriptional Regulation by TP53
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Literatures that report relations between FAS and anti-tumor immunity. The specific mechanism were also collected if the literature reports that a gene specifically promotes or inhibits the infiltration or function of T/NK cells.
> Text Mining
 
  Literatures describing the relation between FAS and anti-tumor immunity in human cancer.
PMID Cancer type Relation to immunity Evidence sentences
26136424Colon CarcinomaPromote immunity (T cell function)Using an orthotopic colon cancer mouse model, we demonstrated that tumor-infiltrating cytotoxic T lymphocytes are FasL(+) and that FasL-mediated cancer immune surveillance is essential for colon carcinoma growth control in vivo. Our findings determine that H3K9me3 of the FAS promoter is a dominant mechanism underlying FAS silencing and resultant colon carcinoma immune evasion and progression.
10706715Lung CarcinomaPromote immunityThe finding of up-regulated CD95 expression on tumor cells placed in vivo suggests that a CD95-based mechanism plays a role in tumor immunity at early stages of tumor growth. Consequently, the progressive down-regulation of CD95 expression during tumor progression may indeed be an escape mechanism as previously reported.
24487434Diffuse Large B Cell LymphomaPromote immunity (T cell function); increase the efficacy of immunotherapyFas ligand-mediated immune surveillance by T cells is essential for the control of spontaneous B cell lymphomas. Impairment of T cell control results in rapid development of DLBCL-like disease, which can be eradicated by polyclonal CD8(+) T cells in a T cell receptor-, CD28- and Fas ligand-dependent manner.
19265159Lung carcinomaInhibit immunityTherefore, our results demonstrate that Fas signal can promote lung cancer growth by recruiting MDSC via cancer cell-derived PGE(2), thus providing new mechanistic explanation for the role of inflammation in cancer progression and immune escape.
23390011Colon CarcinomaInhibit immunity (infiltration)PGE2 signals through four different receptors (EP1-EP4) and targeting individual receptor(s) may avoid these side effects, while retaining significant anticancer benefits. This antitumor effect was associated with reduced Fas ligand expression and attenuated tumor-induced immune suppression. In particular, tumor infiltration by CD4(+) CD25(+) Foxp3(+) regulatory T cells was decreased, whereas the cytotoxic activity of isolated splenocytes against CT26 cells was increased.
21278794Breast CarcinomaPromote immunitySecretion of pro-inflammatory cytokines by the senescent cells, particularly TNF-α and IFN-γ, mediates Fas upregulation. Indeed, treatment of proliferating cancer cell lines with TNF-α and IFN-γ, upregulates Fas expression, while blocking TNF-α and IFN-γ by using neutralizing antibodies, decreases Fas expression in senescent cells. We also demonstrate that NF-κB has a central role in controlling the senescence-associated secretory phenotype (SASP) by the premature senescent cells, and that TNF-α and IFN-γ, transcriptionally controlled by NF-κB, are the main mediators of Fas upregulation. Our data suggest the existence of an NF-κB-dependent autocrine loop, mediated by TNF-α and IFN-γ, responsible for expression of Fas on the surface of senescent cells, and for their killing.
19692638Head and Neck Squamous Cell CarcinomaInhibit immunity (T cell function)Sera of patients with cancer contain membraneous microvesicles (MV) able to induce apoptosis of activated T cells by activating the Fas/Fas ligand pathway.
24808361Renal Cell CarcinomaPromote immunityWe demonstrate in this study in two murine tumor models that Treg and MDSC loss within the tumor microenvironment after IL-2/αCD40 occurs through a Fas-dependent cell death pathway. Among tumor-infiltrating leukocytes, CD8(+) T cells, neutrophils, and immature myeloid cells expressed Fas ligand after treatment. Fas was expressed by tumor-associated Tregs and immature myeloid cells, including MDSCs. Tregs and MDSCs in the tumor microenvironment expressed active caspases after IL-2/αCD40 therapy and, in contrast with effector T cells, Tregs significantly downregulated Bcl-2 expression. Adoptive transfer of Fas-deficient Tregs or MDSCs into wild-type, Treg-, or MDSC-depleted hosts resulted in the persistence of Tregs or MDSCs and the loss of antitumor efficacy in response to IL-2/αCD40. These results demonstrate the importance of Fas-mediated Treg/MDSC removal for successful antitumor immunotherapy.
25012502Pancreatic ductal adenocarcinomaPromote immunity (T cell function)Tumor cells treated with sublethal doses of RLH ligands upregulated Fas and MHC-I expression and were effectively sensitized towards Fas-mediated apoptosis and cytotoxic T lymphocyte (CTL)-mediated lysis.
24004671Plasma Cell MyelomaPromote immunity (T cell function)Further analyses revealed that adhesion to accessory cells downregulated Fas and upregulated the caspase-3 inhibitor survivin in multiple myeloma cells. Reconstitution of Fas expression with bortezomib enhanced the CTL-mediated lysis of multiple myeloma cells.
21321117Chronic myelogenous leukemiaPromote immunity (NK cell function)Overexpression of IL-32alpha increases natural killer cell-mediated killing through up-regulation of Fas and UL16-binding protein 2 (ULBP2) expression in human chronic myeloid leukemia cells. Taken together, these data show that IL-32α stimulates Fas and ULBP2 expression via activation of p38 MAPK, which increases NK susceptibility of CML cells. Enhanced NK cell susceptibility of CML cells by IL-32α overexpression may improve the efficiency of NK cell-based immunotherapy.
15981207Cervical CarcinomaPromote immunity (T cell function)Our results demonstrated that chimeric CRT/E7 DNA vaccine resulted in control of tumors with downregulated Fas expression, highlighting the importance of the Fas-FasL pathway in the potent antitumor effect of antigen-specific CD8+ cytotoxic T lymphocytes and the role of Fas as part of in vivo tumor evasion.
29123081MelanomaInhibit immunityApoptosis of tumor-infiltrating lymphocytes can be prevented by interrupting the Fas/Fas-ligand axis, and is triggered by polymorphonuclear-myeloid-derived suppressor cells, which express high levels of Fas-ligand and are enriched in TiRP tumors. Blocking Fas-ligand increases the anti-tumor efficacy of adoptive T-cell therapy in TiRP tumors, and increases the efficacy of checkpoint blockade in transplanted tumors.
22027835Colon CarcinomaPromote immunityBinding of TRAIL and CD95 ligand to their cognate receptors primarily leads to formation of a complex comprising the receptor, FADD, and caspase-8, referred to as the death-inducing signaling complex (DISC).
21622855MelanomaPromote immunityRemarkably, in vivo protection of T cells from TCR-mediated apoptosis by an adenovirus engineered to produce soluble Fas resulted in a dramatic reduction in tumor growth.
25248763E.G7-OVA tumorsPromote immunity (T cell function)Bone marrow chimeras revealed that IFNgammaR1 and Fas expression on immune cells was most critical for rejection, and SPLNX increased the frequency of activated macrophages (Mvarphi) within intraocular tumors in an IFNgamma- and Fas/FasL-dependent manner, suggesting an immune cell target of IFNgamma and Fas. As depletion of Mvarphis limited CD8 T cell-mediated rejection of intraocular tumors in SPLNX mice, our data support a model in which IFNgamma- and Fas/FasL-dependent activation of intratumoral Mvarphis by CD8(+) T cells promotes severe intraocular inflammation that indirectly eliminates intraocular tumors by inducing phthisis, and suggests that immunosuppressive mechanisms that maintain ocular IP interfere with the interaction between CD8(+) T cells and Mvarphis to limit the immunosurveillance of intraocular tumors.
23341634fibrosarcoma; MelanomaPromote immunityComplete tumor rejection required IFNgamma-regulated Fas by the tumor stroma. Therefore, T(E) cells lacking IFNgamma or FasL cannot prevent progression of antigenic cancer because the tumor stroma escapes destruction if its Fas expression is down-regulated.
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content High-throughput screening data (e.g. CRISPR-Cas9, shRNA and RNAi) for T cell-mediated killing. Genetic screen techniques can identify mechanisms of tumor cell resistance (e.g., PTPN2) and sensitivity (e.g., APLNR) to killing by cytotoxic T cells, the central effectors of anti-tumor immunity. After comprehensively searching, eight groups of screening data sets were collected in the current database. In this tab, users can check whether their selected genes cause resistance or increase sensitivity to T cell-mediated killing in various data sets.
> High-throughput Screening
  Statistical results of FAS in screening data sets for detecting immune reponses.
PMID Screening System Cancer Type Cell Line Data Set Statistical Results Relation to immunity
29301958CRISPR-Cas9 melanomaB16F10Pmel-1 T cell NA/NSNA/NS
29301958CRISPR-Cas9 melanomaB16F10OT-1 T cell NA/NSNA/NS
28783722CRISPR-Cas9 melanomaMel6242CT-CRISPR NA/NSNA/NS
28723893CRISPR-Cas9 melanomaB16GVAX+Anti-PD1 NA/NSNA/NS
28723893CRISPR-Cas9 melanomaB16GVAX NA/NSNA/NS
25691366RNAiBreast cancerMCF7Luc-CTL assay NA/NSNA/NS
24476824shRNAmelanomaB16Primary screen NA/NSNA/NS
24476824shRNAmelanomaB16Secondary screen NA/NSNA/NS
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Transcriptomic and genomic profiling of pre-treated tumor biopsies from responders and non-responders to immunotherapy. These data were used to identify signatures and mechanisms of response to checkpoint blockade (e.g., anti-PDL1 and anti-PD1). One example is that mutations in the gene PBRM1 benefit clinical survival of patients with clear cell renal cell carcinoma. After comprehensively searching, we collected 5 and 6 of transcriptomic and genomic data sets, respectively. In this tab, users can check whether their selected genes have significant difference of expression or mutation between responders and non-responders in various data sets.
> Expression difference between responders and non-responders
> Mutation difference between responders and non-responders
> Expression difference between responders and non-responders
 
Points in the above scatter plot represent the expression difference of FAS in various data sets.
No PMID Cancer type Group Drug # Res # NRes Log2 (Fold Change) P value Anno
126997480MelanomaallAnti-PD-1 (pembrolizumab and nivolumab)14120.010.983
226997480MelanomaMAPKiAnti-PD-1 (pembrolizumab and nivolumab)65-0.5560.683
326997480Melanomanon-MAPKiAnti-PD-1 (pembrolizumab and nivolumab)870.4180.707
428552987Urothelial cancerallAnti-PD-L1 (atezolizumab) 916-0.4320.293
528552987Urothelial cancersmokingAnti-PD-L1 (atezolizumab) 59-0.9420.487
628552987Urothelial cancernon-smokingAnti-PD-L1 (atezolizumab) 470.2170.903
729033130MelanomaallAnti-PD-1 (nivolumab) 26230.0630.878
829033130MelanomaNIV3-PROGAnti-PD-1 (nivolumab) 1511-0.290.822
929033130MelanomaNIV3-NAIVEAnti-PD-1 (nivolumab) 11120.3810.801
1029301960Clear cell renal cell carcinoma (ccRCC)allAnti-PD-1 (nivolumab) 480.3260.842
1129301960Clear cell renal cell carcinoma (ccRCC)VEGFRiAnti-PD-1 (nivolumab) 2001
1229301960Clear cell renal cell carcinoma (ccRCC)non-VEGFRiAnti-PD-1 (nivolumab) 280.4040.872
1329443960Urothelial cancerallAnti-PD-L1 (atezolizumab) 68230-0.3060.0306
> Mutation difference between responders and non-responders
 
Points in the above scatter plot represent the mutation difference of FAS in various data sets.
No PMID Cancer type Group Drug # Res # NRes % Mut/Res % Mut/NRes % Diff (R vs NR) Pval Anno
125765070Non-small cell lung cancer (NSCLC)allAnti-PD-1 (pembrolizumab) 14170001
225765070Non-small cell lung cancer (NSCLC)smokingAnti-PD-1 (pembrolizumab) 1030001
325765070Non-small cell lung cancer (NSCLC)non-smokingAnti-PD-1 (pembrolizumab) 4140001
426359337MelanomaallAnti-CTLA-4 (ipilimumab) 27733.703.70.27
526359337MelanomaBRAFiAnti-CTLA-4 (ipilimumab) 0140001
626359337Melanomanon-BRAFiAnti-CTLA-4 (ipilimumab) 27593.703.70.314
726997480MelanomaallAnti-PD-1 (pembrolizumab and nivolumab)21170001
826997480MelanomaMAPKiAnti-PD-1 (pembrolizumab and nivolumab)860001
926997480Melanomanon-MAPKiAnti-PD-1 (pembrolizumab and nivolumab)13110001
1028552987Urothelial cancerallAnti-PD-L1 (atezolizumab) 9160001
1128552987Urothelial cancersmokingAnti-PD-L1 (atezolizumab) 590001
1228552987Urothelial cancernon-smokingAnti-PD-L1 (atezolizumab) 470001
1329033130MelanomaallAnti-PD-1 (nivolumab) 38270001
1429033130MelanomaNIV3-PROGAnti-PD-1 (nivolumab) 22130001
1529033130MelanomaNIV3-NAIVEAnti-PD-1 (nivolumab) 16140001
1629301960Clear cell renal cell carcinoma (ccRCC)allAnti-PD-1 (nivolumab) 11130001
1729301960Clear cell renal cell carcinoma (ccRCC)VEGFRiAnti-PD-1 (nivolumab) 610001
1829301960Clear cell renal cell carcinoma (ccRCC)non-VEGFRiAnti-PD-1 (nivolumab) 5120001
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Relations between abundance of tumor-infiltrating lymphocytes (TILs) and expression, copy number, methylation, or mutation of FAS. The immune-related signatures of 28 TIL types from Charoentong's study, which can be viewed in the download page. For each cancer type, the relative abundance of TILs were inferred by using gene set variation analysis (GSVA) based on gene expression profile. In this tab, users can examine which kinds of TILs might be regulated by the current gene.
> Lymphocyte
 
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Relations between three kinds of immunomodulators and expression, copy number, methylation, or mutation of FAS. These immunomo-dulators were collected from Charoentong's study. In this tab, users can examine which immunomodulators might be regulated by FAS.
> Immunoinhibitor
> Immunostimulator
> MHC molecule
> Immunoinhibitor
 
> Immunostimulator
 
> MHC molecule
 
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Relations between chemokines (or receptors) and expression, copy number, methylation, or mutation of FAS. In this tab, users can examine which chemokines (or receptors) might be regulated by the current gene.
> Chemokine
> Receptor
> Chemokine
 
> Receptor
 
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Distribution of FAS expression across immune and molecular subtypes.
> Immune subtype
> Molecular subtype
> Immune subtype
 
> Molecular subtype
 
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Associations between FAS and clinical features.
> Overall survival analysis
> Cancer stage
> Tumor grade
> Overall survival
 
> Stage
 
> Grade
 
Summary
SymbolFAS
NameFas cell surface death receptor
Aliases CD95; APO-1; TNF receptor superfamily member 6; FAS1; TNFRSF6; tumor necrosis factor receptor superfamily, m ......
Chromosomal Location10q24.1
External Links HGNC, NCBI, Ensembl, Uniprot, GeneCards
Content Drugs targeting FAS collected from DrugBank database.
> Drugs from DrugBank database
 

There is no record.