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Protein Page:
Fas (human)
p Phosphorylation
ac Acetylation
me Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
ub Ubiquitination
sm Sumoylation
ne Neddylation
gl O-GlcNAc
ga O-GalNAc
pa Palmitoylation
ad Adenylylation
sn S-Nitrosylation
ca Caspase cleavage
sc Succinylation

Overview
Fas 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). Binds DAXX. Interacts with HIPK3. Part of a complex containing HIPK3 and FADD. Binds RIPK1 and FAIM2. Interacts with BRE and FEM1B. Interacts with FADD. Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6. 6 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Receptor, cytokine; Membrane protein, integral; Apoptosis; Cell surface
Cellular Component: cell surface; cytoplasm; integral to membrane; plasma membrane; CD95 death-inducing signaling complex; nucleus; cytosol; external side of plasma membrane; lipid raft
Molecular Function: identical protein binding; protein binding; signal transducer activity; transmembrane receptor activity; receptor activity; kinase binding
Biological Process: spleen development; caspase activation; regulation of myeloid cell differentiation; renal system process; transformed cell apoptosis; apoptosis; positive regulation of apoptosis; positive regulation of protein homooligomerization; regulation of lymphocyte differentiation; response to toxin; response to glucocorticoid stimulus; negative regulation of B cell activation; signal transduction; negative thymic T cell selection; regulation of apoptosis; inflammatory cell apoptosis; B cell mediated immunity; induction of apoptosis via death domain receptors; protein complex assembly; immunoglobulin production; activated T cell apoptosis; protein homooligomerization; negative regulation of apoptosis
Reference #:  P25445 (UniProtKB)
Alt. Names/Synonyms: ALPS1A; APO-1; Apo-1 antigen; APO-1 cell surface antigen; apoptosis antigen 1; Apoptosis-mediating surface antigen FAS; APT1; CD95; CD95 antigen; FAS; Fas (TNF receptor superfamily, member 6); Fas AMA; Fas antigen; FAS1; FASLG receptor; FASTM; TNFRSF6; TNR6; Tumor necrosis factor receptor superfamily member 6; tumor necrosis factor receptor superfamily, member 6
Gene Symbols: FAS
Molecular weight: 37,732 Da
Basal Isoelectric point: 8.29  Predict pI for various phosphorylation states
CST Pathways:  Death Receptor Signaling  |  Mitochondrial Control of Apoptosis
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
Select Structure to View Below

Fas

Protein Structure Not Found.


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Sites Implicated In
apoptosis, altered: Y91‑p, Y232‑p, Y291‑p
intracellular localization: Y91‑p, Y232‑p, Y291‑p
molecular association, regulation: Y232‑p, Y291‑p

Modification Sites and Domains Show Modification Legend
Click here to view phosphorylation modifications only

Modification Sites in Parent Protein, Orthologs, and Isoforms Show Modification Legend
 

Show Multiple Sequence Alignment


 SS 

SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.


 MS 

MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.


       human

► Hide Isoforms
 
0 1 T40-ga KGLELRKtVttVEtQ
0 1 T42-ga LELRKtVttVEtQNL
0 1 T43-ga ELRKtVttVEtQNLE
0 1 T46-ga KtVttVEtQNLEGLH
0 1 - gap
0 1 - gap
0 1 H53 tQNLEGLHHDGQFCH
2 0 Y91-p PCQEGKEyTDKAHFS
0 1 K191 IPLIVWVKRKEVQKT
0 3 S209-p HRKENQGsHEsPtLN
0 2 S212-p ENQGsHEsPtLNPEt
0 3 T214-p QGsHEsPtLNPEtVA
0 1 L215 GsHEsPtLNPEtVAI
0 1 N216 sHEsPtLNPEtVAIN
0 3 T219-p sPtLNPEtVAINLSD
0 4 S225 EtVAINLSDVDLSKy
0 5 D228 AINLSDVDLSKyItT
0 3 S230 NLSDVDLSKyItTIA
2 0 Y232-p SDVDLSKyItTIAGV
0 1 T234-p VDLSKyItTIAGVMt
0 1 T241-p tTIAGVMtLsQVKGF
0 1 S243-p IAGVMtLsQVKGFVR
0 1 K246 VMtLsQVKGFVRKNG
0 1 K263-ub EAKIDEIkNDNVQDT
0 1 K288-ub WHQLHGKkEAyDTLI
3 0 Y291-p LHGKkEAyDTLIKDL
0 8 K316-ub KIQTIILkDITSDsE
0 5 S322-p LkDITSDsENsNFRN
0 1 S325-p ITSDsENsNFRNEIQ
0 1 S333-p NFRNEIQsLV_____
  Fas iso6  
T40 KGLELRKTVTTVETQ
T42 LELRKTVTTVETQNL
T43 ELRKTVTTVETQNLE
T46 KTVTTVETQNLEGLH
- gap
- gap
H53 TQNLEGLHHDGQFCH
Y91 PCQEGKEYTDKAHFS
K170-ac TKCKEEVkRKEVQKT
S188 HRKENQGSHESPTLN
S191 ENQGSHESPTLNPET
T193 QGSHESPTLNPETVA
L194 GSHESPTLNPETVAI
N195 SHESPTLNPETVAIN
T198 SPTLNPETVAINLSD
S204 ETVAINLSDVDLSKY
D207 AINLSDVDLSKYITT
S209 NLSDVDLSKYITTIA
Y211 SDVDLSKYITTIAGV
T213 VDLSKYITTIAGVMT
T220 TTIAGVMTLSQVKGF
S222 IAGVMTLSQVKGFVR
K225 VMTLSQVKGFVRKNG
K242 EAKIDEIKNDNVQDT
K267 WHQLHGKKEAYDTLI
Y270 LHGKKEAYDTLIKDL
K295 KIQTIILKDITSDSE
S301 LKDITSDSENSNFRN
S304 ITSDSENSNFRNEIQ
S312 NFRNEIQSLV_____
  mouse

 
- gap
- gap
- gap
- gap
T40-p LRRRVREtDKNCsEG
S45-p REtDKNCsEGLyQGG
Y49-p KNCsEGLyQGGPFCC
Y87 PCTEGKEYMDKNHYA
- gap
- gap
S204-p RRQDDPEsRtssREt
T206-p QDDPEsRtssREtIP
S207-p DDPEsRtssREtIPM
S208-p DPEsRtssREtIPMN
T211-p sRtssREtIPMNAsN
S217-p EtIPMNAsNLsLsKY
S220-p PMNAsNLsLsKYIPR
S222-p NAsNLsLsKYIPRIA
Y224 sNLsLsKYIPRIAED
P226 LsLsKYIPRIAEDMT
T233 PRIAEDMTIQEAkKF
Q235 IAEDMTIQEAkKFAR
K238-ub DMTIQEAkKFARENN
M255 EGKIDEIMHDSIQDT
S280 WYQSHGKSDAYQDLI
Y283 SHGKSDAYQDLIKGL
K308 KFQDMVQKDLGKStP
T314-p QKDLGKStPDtGNEN
T317-p LGKStPDtGNENEGQ
C325 GNENEGQCLE_____
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