SELE
E-selectin
Also known as: CD62E, ELAM, ELAM1, ESEL, LYAM2_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P16581
- Gene
- SELE
- Ensembl
- ENSG00000007908
- Chromosome
- 1
- Canonical length
- 610 aa
- Protein class
- Cancer-related genes, Candidate cardiovascular disease genes, CD markers, Plasma proteins, Predicted intracellular proteins, Predicted membrane proteins
OverviewNCBI Gene
The protein encoded by this gene is found in cytokine-stimulated endothelial cells and is thought to be responsible for the accumulation of blood leukocytes at sites of inflammation by mediating the adhesion of cells to the vascular lining. It exhibits structural features such as the presence of lectin- and EGF-like domains followed by short consensus repeat (SCR) domains that contain 6 conserved cysteine residues. These proteins are part of the selectin family of cell adhesion molecules. Adhesion molecules participate in the interaction between leukocytes and the endothelium and appear to be involved in the pathogenesis of atherosclerosis. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
610 residues, UniProt reviewed canonical sequence.
>P16581|SELE
1 MIASQFLSAL TLVLLIKESG AWSYNTSTEA MTYDEASAYC QQRYTHLVAI QNKEEIEYLN
61 SILSYSPSYY WIGIRKVNNV WVWVGTQKPL TEEAKNWAPG EPNNRQKDED CVEIYIKREK
121 DVGMWNDERC SKKKLALCYT AACTNTSCSG HGECVETINN YTCKCDPGFS GLKCEQIVNC
181 TALESPEHGS LVCSHPLGNF SYNSSCSISC DRGYLPSSME TMQCMSSGEW SAPIPACNVV
241 ECDAVTNPAN GFVECFQNPG SFPWNTTCTF DCEEGFELMG AQSLQCTSSG NWDNEKPTCK
301 AVTCRAVRQP QNGSVRCSHS PAGEFTFKSS CNFTCEEGFM LQGPAQVECT TQGQWTQQIP
361 VCEAFQCTAL SNPERGYMNC LPSASGSFRY GSSCEFSCEQ GFVLKGSKRL QCGPTGEWDN
421 EKPTCEAVRC DAVHQPPKGL VRCAHSPIGE FTYKSSCAFS CEEGFELHGS TQLECTSQGQ
481 WTEEVPSCQV VKCSSLAVPG KINMSCSGEP VFGTVCKFAC PEGWTLNGSA ARTCGATGHW
541 SGLLPTCEAP TESNIPLVAG LSAAGLSLLT LAPFLLWLRK CLRKAKKFVP ASSCQSLESD
601 GSYQKPSYILLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SELE 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)
- 0.37
- Highest tissue expression
- 52 nTPM
Expression across tissuesHPA
Tissue
- urinary bladder: 52 nTPM
- adipose tissue: 28 nTPM
- prostate: 26 nTPM
- fallopian tube: 21 nTPM
- smooth muscle: 18 nTPM
- thyroid gland: 13 nTPM
Single-cell type
- vascular endothelial cells: 802 nCPM
- lymphatic endothelial cells: 30 nCPM
- thymic myoid cells: 14 nCPM
- hepatocytes: 12 nCPM
- salivary myoepithelial cells: 7.1 nCPM
- late spermatids: 5 nCPM
Immune cell
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- eosinophil: 0 nTPM
- gdT-cell: 0 nTPM
- intermediate monocyte: 0 nTPM
- MAIT T-cell: 0 nTPM
Brain region
- choroid plexus: 7.9 nTPM
- thalamus: 5.5 nTPM
- cerebral cortex: 3.4 nTPM
- medulla oblongata: 3.3 nTPM
- pons: 3 nTPM
- hypothalamus: 2.5 nTPM
ReferencesPubMed · IEDB
Publications for SELE from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.
Reference: AutoantibodyPubMed
1 publication
- A novel model for the pre-clinical imaging of inflamed human synovial vasculature.
2009 · Rheumatology (Oxford) · RCR 0.4 · 15 citations
Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.
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)
- 0.86
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.13
- DepMap mean gene effect
- 0.02
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- actin filament-based process
- calcium-mediated signaling
- heterophilic cell-cell adhesion via plasma membrane cell adhesion molecules
- inflammatory response
- leukocyte cell-cell adhesion
- leukocyte migration involved in inflammatory response
- leukocyte tethering or rolling
- phospholipase C-activating G protein-coupled receptor signaling pathway
- positive regulation of leukocyte migration
- positive regulation of leukocyte tethering or rolling
- positive regulation of receptor internalization
- regulation of inflammatory response
- response to cytokine
- response to interleukin-1
- response to lipopolysaccharide
- response to tumor necrosis factor
Molecular functions
- metal ion binding
- oligosaccharide binding
- phospholipase binding
- sialic acid binding
- transmembrane signaling receptor activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of SELE 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 SELE as an antibody target. Whether an autoantibody or antibody against SELE could matter depends on whether native SELE is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SELE is annotated at the cell surface, where native SELE 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 SELE as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
Loading the interactive Seroatlas protein explorer...