CLEC4F
C-type lectin domain family 4 member F
Also known as: CLC4F_HUMAN, CLECSF13, FLJ39110, KCLR
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q8N1N0
- Gene
- CLEC4F
- Ensembl
- ENSG00000152672
- Chromosome
- 2
- Canonical length
- 589 aa
- Protein class
- Predicted membrane proteins
- Subcellular location
- Plasma membrane,Cytosol
OverviewNCBI Gene
Predicted to enable galactose binding activity; glycolipid binding activity; and pattern recognition receptor activity. Predicted to be involved in immune response. Predicted to act upstream of or within NK T cell activation. Predicted to be located in plasma membrane. Predicted to be active in external side of plasma membrane. [provided by Alliance of Genome Resources, Jul 2025]
Canonical amino-acid sequenceUniProt
589 residues, UniProt reviewed canonical sequence.
>Q8N1N0|CLEC4F
1 MDGEAVRFCT DNQCVSLHPQ EVDSVAMAPA APKIPRLVQA TPAFMAVTLV FSLVTLFVVV
61 QQQTRPVPKP VQAVILGDNI TGHLPFEPNN HHHFGREAEM RELIQTFKGH MENSSAWVVE
121 IQMLKCRVDN VNSQLQVLGD HLGNTNADIQ MVKGVLKDAT TLSLQTQMLR SSLEGTNAEI
181 QRLKEDLEKA DALTFQTLNF LKSSLENTSI ELHVLSRGLE NANSEIQMLN ASLETANTQA
241 QLANSSLKNA NAEIYVLRGH LDSVNDLRTQ NQVLRNSLEG ANAEIQGLKE NLQNTNALNS
301 QTQAFIKSSF DNTSAEIQFL RGHLERAGDE IHVLKRDLKM VTAQTQKANG RLDQTDTQIQ
361 VFKSEMENVN TLNAQIQVLN GHMKNASREI QTLKQGMKNA SALTSQTQML DSNLQKASAE
421 IQRLRGDLEN TKALTMEIQQ EQSRLKTLHV VITSQEQLQR TQSQLLQMVL QGWKFNGGSL
481 YYFSSVKKSW HEAEQFCVSQ GAHLASVASK EEQAFLVEFT SKVYYWIGLT DRGTEGSWRW
541 TDGTPFNAAQ NKAPGSKGSC PLRKYIIVNS GMGACSFIDT PPCPWILSNLocalizationUniProt · AlphaFold · HPA
Whether an antibody against CLEC4F 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)
- 0.5
- Highest tissue expression
- 16 nTPM
Expression across tissuesHPA
Tissue
- retina: 16 nTPM
- small intestine: 4.2 nTPM
- spleen: 3.2 nTPM
- cervix: 1.6 nTPM
- salivary gland: 1.6 nTPM
- adipose tissue: 1.5 nTPM
Single-cell type
- cdc: 22 nCPM
- rod photoreceptor cells: 17 nCPM
- cone photoreceptor cells: 12 nCPM
- retinal ganglion cells: 7.7 nCPM
- macrophages: 7.1 nCPM
- retinal horizontal cells: 4 nCPM
Immune cell
- intermediate monocyte: 6 nTPM
- non-classical monocyte: 4.4 nTPM
- myeloid DC: 0.4 nTPM
- total PBMC: 0.3 nTPM
- classical monocyte: 0.2 nTPM
- basophil: 0 nTPM
Brain region
- cerebral cortex: 0.3 nTPM
- cerebellum: 0.2 nTPM
- hypothalamus: 0.2 nTPM
- pons: 0.2 nTPM
- amygdala: 0.1 nTPM
- basal ganglia: 0.1 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)
- 1.31
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.26
- DepMap mean gene effect
- -0.08
- 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
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads CLEC4F as an antibody target. Whether an autoantibody or antibody against CLEC4F could matter depends on whether native CLEC4F is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CLEC4F is annotated at the cell surface, where native CLEC4F 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 CLEC4F as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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