FES
Tyrosine-protein kinase Fes/Fps
Also known as: FES_HUMAN, FPS
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P07332
- Gene
- FES
- Ensembl
- ENSG00000182511
- Chromosome
- 15
- Canonical length
- 822 aa
- Protein class
- Cancer-related genes, Disease related genes, Enzymes, Potential drug targets, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Vesicles,Cytosol
- Quaternary structure
- Homooligomer
OverviewNCBI Gene
This gene encodes the human cellular counterpart of a feline sarcoma retrovirus protein with transforming capabilities. The gene product has tyrosine-specific protein kinase activity and that activity is required for maintenance of cellular transformation. Its chromosomal location has linked it to a specific translocation event identified in patients with acute promyelocytic leukemia but it is also involved in normal hematopoiesis as well as growth factor and cytokine receptor signaling. Alternative splicing results in multiple variants encoding different isoforms.[provided by RefSeq, Jan 2009]
Canonical amino-acid sequenceUniProt
822 residues, UniProt reviewed canonical sequence.
>P07332|FES
1 MGFSSELCSP QGHGVLQQMQ EAELRLLEGM RKWMAQRVKS DREYAGLLHH MSLQDSGGQS
61 RAISPDSPIS QSWAEITSQT EGLSRLLRQH AEDLNSGPLS KLSLLIRERQ QLRKTYSEQW
121 QQLQQELTKT HSQDIEKLKS QYRALARDSA QAKRKYQEAS KDKDRDKAKD KYVRSLWKLF
181 AHHNRYVLGV RAAQLHHQHH HQLLLPGLLR SLQDLHEEMA CILKEILQEY LEISSLVQDE
241 VVAIHREMAA AAARIQPEAE YQGFLRQYGS APDVPPCVTF DESLLEEGEP LEPGELQLNE
301 LTVESVQHTL TSVTDELAVA TEMVFRRQEM VTQLQQELRN EEENTHPRER VQLLGKRQVL
361 QEALQGLQVA LCSQAKLQAQ QELLQTKLEH LGPGEPPPVL LLQDDRHSTS SSEQEREGGR
421 TPTLEILKSH ISGIFRPKFS LPPPLQLIPE VQKPLHEQLW YHGAIPRAEV AELLVHSGDF
481 LVRESQGKQE YVLSVLWDGL PRHFIIQSLD NLYRLEGEGF PSIPLLIDHL LSTQQPLTKK
541 SGVVLHRAVP KDKWVLNHED LVLGEQIGRG NFGEVFSGRL RADNTLVAVK SCRETLPPDL
601 KAKFLQEARI LKQYSHPNIV RLIGVCTQKQ PIYIVMELVQ GGDFLTFLRT EGARLRVKTL
661 LQMVGDAAAG MEYLESKCCI HRDLAARNCL VTEKNVLKIS DFGMSREEAD GVYAASGGLR
721 QVPVKWTAPE ALNYGRYSSE SDVWSFGILL WETFSLGASP YPNLSNQQTR EFVEKGGRLP
781 CPELCPDAVF RLMEQCWAYE PGQRPSFSTI YQELQSIRKR HRLocalizationUniProt · AlphaFold · HPA
Whether an antibody against FES 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
- 0
- Mean surface accessibility (rSASA)
- 0.33
- Highest tissue expression
- 110 nTPM
Expression across tissuesHPA
Tissue
- spleen: 110 nTPM
- bone marrow: 79 nTPM
- salivary gland: 55 nTPM
- lung: 30 nTPM
- adipose tissue: 30 nTPM
- liver: 25 nTPM
Single-cell type
- neutrophils: 128 nCPM
- neutrophil progenitors: 120 nCPM
- tuft cells: 104 nCPM
- kupffer cells: 103 nCPM
- monocytes: 97 nCPM
- hofbauer cells: 84 nCPM
Immune cell
- eosinophil: 317 nTPM
- myeloid DC: 163 nTPM
- classical monocyte: 152 nTPM
- neutrophil: 101 nTPM
- intermediate monocyte: 89 nTPM
- total PBMC: 81 nTPM
Brain region
- medulla oblongata: 12 nTPM
- thalamus: 12 nTPM
- spinal cord: 11 nTPM
- pons: 10 nTPM
- cerebral cortex: 10 nTPM
- white matter: 9.6 nTPM
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)
- 0.85
- gnomAD pLI
- 0
- gnomAD missense Z
- 1.76
- DepMap mean gene effect
- -0.13
- DepMap dependency class
- selective
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
- cardiac muscle cell proliferation
- cell adhesion
- cellular response to vitamin D
- centrosome cycle
- chemotaxis
- microtubule bundle formation
- myoblast proliferation
- peptidyl-tyrosine phosphorylation
- positive regulation of microtubule polymerization
- positive regulation of monocyte differentiation
- positive regulation of myeloid cell differentiation
- positive regulation of neuron projection development
- protein autophosphorylation
- regulation of cell adhesion
- regulation of cell differentiation
- regulation of cell motility
- regulation of cell population proliferation
- regulation of cell shape
- regulation of mast cell degranulation
- regulation of vesicle-mediated transport
Molecular functions
- ATP binding
- immunoglobulin receptor binding
- microtubule binding
- non-membrane spanning protein tyrosine kinase activity
- phosphatidylinositol binding
- protein tyrosine kinase activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Protein kinase domain
- SH2 domain
- FCH domain
- Serine-threonine/tyrosine-protein kinase, catalytic domain
- Tyrosine-protein kinase, active site
- Protein kinase-like domain superfamily
- Tyrosine-protein kinase, Fes/Fps type
- Protein kinase, ATP binding site
- Tyrosine-protein kinase, catalytic domain
- AH/BAR domain superfamily
- F-BAR domain
- Fes/Fps/Fer, SH2 domain
- SH2 domain superfamily
- Non-receptor tyrosine kinases involved in cell signaling
- SH2 domain
- Fes/CIP4, and EFC/F-BAR homology domain
- Protein tyrosine and serine/threonine kinase
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of FES 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 FES as an antibody target. Whether an autoantibody or antibody against FES could matter depends on whether native FES is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
FES is annotated at the cell surface, where native FES 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 FES as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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