SLAMF8
SLAM family member 8
Also known as: BLAME, CD353, SBBI42, SLAF8_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9P0V8
- Gene
- SLAMF8
- Ensembl
- ENSG00000158714
- Chromosome
- 1
- Canonical length
- 285 aa
- Protein class
- CD markers, Predicted membrane proteins
OverviewNCBI Gene
This gene encodes a member of the CD2 family of cell surface proteins involved in lymphocyte activation. These proteins are characterized by Ig domains. This protein is expressed in lymphoid tissues, and studies of a similar protein in mouse suggest that it may function during B cell lineage commitment. The gene is found in a region of chromosome 1 containing many CD2 genes. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
285 residues, UniProt reviewed canonical sequence.
>Q9P0V8|SLAMF8
1 MVMRPLWSLL LWEALLPITV TGAQVLSKVG GSVLLVAARP PGFQVREAIW RSLWPSEELL
61 ATFFRGSLET LYHSRFLGRA QLHSNLSLEL GPLESGDSGN FSVLMVDTRG QPWTQTLQLK
121 VYDAVPRPVV QVFIAVERDA QPSKTCQVFL SCWAPNISEI TYSWRRETTM DFGMEPHSLF
181 TDGQVLSISL GPGDRDVAYS CIVSNPVSWD LATVTPWDSC HHEAAPGKAS YKDVLLVVVP
241 VSLLLMLVTL FSAWHWCPCS GKKKKDVHAD RVGPETENPL VQDLPLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SLAMF8 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)
- 0.4
- Highest tissue expression
- 31 nTPM
Expression across tissuesHPA
Tissue
- lymph node: 31 nTPM
- appendix: 28 nTPM
- tonsil: 17 nTPM
- lung: 15 nTPM
- spleen: 11 nTPM
- thymus: 9.8 nTPM
Single-cell type
- cdc: 66 nCPM
- macrophages: 38 nCPM
- cardiomyocytes: 18 nCPM
- kupffer cells: 13 nCPM
- monocytes: 13 nCPM
- hofbauer cells: 12 nCPM
Immune cell
- myeloid DC: 14 nTPM
- NK-cell: 8.9 nTPM
- intermediate monocyte: 8 nTPM
- classical monocyte: 5.8 nTPM
- memory CD8 T-cell: 4.6 nTPM
- gdT-cell: 3.5 nTPM
Brain region
- thalamus: 14 nTPM
- pons: 7.5 nTPM
- medulla oblongata: 6.7 nTPM
- white matter: 6.6 nTPM
- choroid plexus: 3.7 nTPM
- spinal cord: 2.8 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)
- 1.19
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.29
- DepMap mean gene effect
- -0.04
- 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
- defense response to bacterium
- immune response
- leukocyte chemotaxis involved in inflammatory response
- negative regulation of macrophage chemotaxis
- negative regulation of monocyte chemotaxis
- negative regulation of respiratory burst involved in inflammatory response
- phagosome acidification
- regulation of B cell differentiation
- B-1 B cell lineage commitment
- negative regulation of dendritic cell chemotaxis
- negative regulation of neutrophil migration
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads SLAMF8 as an antibody target. Whether an autoantibody or antibody against SLAMF8 could matter depends on whether native SLAMF8 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SLAMF8 is annotated at the cell surface, where native SLAMF8 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 SLAMF8 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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