FASLG
Tumor necrosis factor ligand superfamily member 6
Also known as: APT1LG1, CD178, FasL, TNFL6_HUMAN, TNFSF6
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P48023
- Gene
- FASLG
- Ensembl
- ENSG00000117560
- Chromosome
- 1
- Canonical length
- 281 aa
- Protein class
- Cancer-related genes, CD markers, Disease related genes, Human disease related genes, Plasma proteins, Potential drug targets, Predicted membrane proteins, Predicted secreted proteins, RAS pathway related proteins, Transporters
- Secretome location
- Secreted to blood
- Quaternary structure
- Homotrimer
OverviewNCBI Gene
This gene is a member of the tumor necrosis factor superfamily. The primary function of the encoded transmembrane protein is the induction of apoptosis triggered by binding to FAS. The FAS/FASLG signaling pathway is essential for immune system regulation, including activation-induced cell death (AICD) of T cells and cytotoxic T lymphocyte induced cell death. It has also been implicated in the progression of several cancers. Defects in this gene may be related to some cases of systemic lupus erythematosus (SLE). Alternatively spliced transcript variants have been described. [provided by RefSeq, Nov 2014]
Canonical amino-acid sequenceUniProt
281 residues, UniProt reviewed canonical sequence.
>P48023|FASLG
1 MQQPFNYPYP QIYWVDSSAS SPWAPPGTVL PCPTSVPRRP GQRRPPPPPP PPPLPPPPPP
61 PPLPPLPLPP LKKRGNHSTG LCLLVMFFMV LVALVGLGLG MFQLFHLQKE LAELRESTSQ
121 MHTASSLEKQ IGHPSPPPEK KELRKVAHLT GKSNSRSMPL EWEDTYGIVL LSGVKYKKGG
181 LVINETGLYF VYSKVYFRGQ SCNNLPLSHK VYMRNSKYPQ DLVMMEGKMM SYCTTGQMWA
241 RSSYLGAVFN LTSADHLYVN VSELSLVNFE ESQTFFGLYK LLocalizationUniProt · AlphaFold · HPA
Whether an antibody against FASLG can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Cell surface
- Secreted
- No
- Transmembrane segments
- 1
- Mean surface accessibility (rSASA)
- 0.46
- Highest tissue expression
- 5.3 nTPM
Expression across tissuesHPA
Tissue
- lymph node: 5.3 nTPM
- spleen: 4 nTPM
- bone marrow: 2.7 nTPM
- lung: 1.8 nTPM
- duodenum: 1.7 nTPM
- tonsil: 1.7 nTPM
Single-cell type
- nk-cells: 53 nCPM
- t-cells: 25 nCPM
- innate lymphoid cells: 3.5 nCPM
- epididymal clear cells: 2 nCPM
- mast cells: 1.3 nCPM
- plasma cells: 0.8 nCPM
Immune cell
- gdT-cell: 58 nTPM
- NK-cell: 42 nTPM
- MAIT T-cell: 36 nTPM
- memory CD8 T-cell: 31 nTPM
- naive CD8 T-cell: 25 nTPM
- total PBMC: 15 nTPM
Brain region
- white matter: 1.5 nTPM
- medulla oblongata: 1.4 nTPM
- midbrain: 1.4 nTPM
- cerebral cortex: 1.3 nTPM
- pons: 1.2 nTPM
- basal ganglia: 1.1 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about FASLG.
Disease | AllUniProt
Conditions FASLG is implicated in, by any mechanism.
- Autoimmune lymphoproliferative syndrome 1B (ALPS1B) MIM:601859
Disease | GeneticClinVar
6 pathogenic / likely-pathogenic of 231 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Autoimmune lymphoproliferative syndrome type 1
- FASLG-Related Autoimmune Lymphoproliferative Syndrome
- Lung cancer
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.72
- gnomAD pLI
- 0.18
- gnomAD missense Z
- 0.58
- DepMap mean gene effect
- 0.11
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- apoptotic process
- apoptotic signaling pathway
- cell-cell signaling
- cellular response to type II interferon
- endosomal lumen acidification
- extrinsic apoptotic signaling pathway
- extrinsic apoptotic signaling pathway via death domain receptors
- inflammatory cell apoptotic process
- intracellular chloride ion homeostasis
- necroptotic process
- necroptotic signaling pathway
- negative regulation of angiogenesis
- negative regulation of transcription by RNA polymerase II
- positive regulation of apoptotic process
- positive regulation of canonical NF-kappaB signal transduction
- positive regulation of cell population proliferation
- positive regulation of endothelial cell apoptotic process
- positive regulation of epidermal growth factor receptor signaling pathway
- positive regulation of extrinsic apoptotic signaling pathway
- positive regulation of neuron apoptotic process
- release of sequestered calcium ion into cytosol by endoplasmic reticulum
- response to growth factor
- response to lipopolysaccharide
- retinal cell programmed cell death
- signal transduction
- T cell apoptotic process
- positive regulation of phosphatidylserine exposure on apoptotic cell surface
Molecular functions
- cytokine activity
- death receptor binding
- signaling receptor binding
- tumor necrosis factor receptor binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Tumour necrosis factor domain
- Tumour necrosis factor
- Tumour necrosis factor-like domain superfamily
- Tumour necrosis factor, conserved site
- TNF(Tumour Necrosis Factor) family
- Tumor necrosis factor ligand superfamily member 6
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of FASLG in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads FASLG as an antibody target. Whether an autoantibody or antibody against FASLG could matter depends on whether native FASLG is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
FASLG is annotated at the cell surface, where native FASLG is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label FASLG as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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