Seroatlas · Human Serome Atlas

SLFNL1

Schlafen-like protein 1

Also known as: FLJ23878, SLNL1_HUMAN

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
Q499Z3
Gene
SLFNL1
Ensembl
ENSG00000171790
Chromosome
1
Canonical length
407 aa
Protein class
Predicted intracellular proteins
Subcellular location
Cytosol

OverviewNCBI Gene

Predicted to enable ATP binding activity. [provided by Alliance of Genome Resources, Jul 2025]

Canonical amino-acid sequenceUniProt

407 residues, UniProt reviewed canonical sequence.

>Q499Z3|SLFNL1
     1  MTPMKRSVQT QVSEPFMESW GEESLPELPA EQSLTEYSDL EEAPSAHTLY VGHLNPQFSV
    61  PVLACLLRDT LERLEMPVAR EHIEVVRRPR KAYALVQVTV HRDTLASLPW RLQTALEEHL
   121  ILKELAARGK DLLLSEAQGP FSHREEKEEE EEDSGLSPGP SPGSGVPLPT WPTHTLPDRP
   181  QAQQLQSCQG RPSGVCSDSA IVHQQIVGKD QLFQGAFLGS ETRNMEFKRG SGEYLSLAFK
   241  HHVRRYVCAF LNSEGGSLLV GVEDSGLVQG IRCSHRDEDR ARLLVDSILQ GFKPQIFPDA
   301  YTLTFIPVIS TSETSVPLKV IRLTVHTPKA QSQPQLYQTD QGEVFLRRDG SIQGPLSASA
   361  IQEWCRQRWL VELGKLEEKM KALMMEKEQL QQQLQQHGPV SCTCCVL

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against SLFNL1 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
Unknown
Secreted
No
Transmembrane segments
0
Mean surface accessibility (rSASA)
0.43
Highest tissue expression
71 nTPM

Expression across tissuesHPA

Tissue

  • testis: 71 nTPM
  • salivary gland: 3.8 nTPM
  • lung: 2 nTPM
  • liver: 1.5 nTPM
  • prostate: 1.4 nTPM
  • ovary: 1.3 nTPM

Single-cell type

  • late spermatids: 1,284 nCPM
  • early spermatids: 309 nCPM
  • enterocytes: 87 nCPM
  • late primary spermatocytes: 70 nCPM
  • cholangiocytes: 70 nCPM
  • hepatic stellate cells: 58 nCPM

Immune cell

  • basophil: 0.2 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 nTPM
  • cerebral cortex: 4.3 nTPM
  • cerebellum: 4.2 nTPM
  • basal ganglia: 3.5 nTPM
  • hypothalamus: 3.5 nTPM
  • amygdala: 3.4 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)
1.08
gnomAD pLI
0
gnomAD missense Z
-0.6
DepMap mean gene effect
-0.3
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

Molecular functions

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads SLFNL1 as an antibody target. Whether an autoantibody or antibody against SLFNL1 could matter depends on whether native SLFNL1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

SLFNL1 is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.

Annotation status

The present source text does not explicitly label SLFNL1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/SLFNL1. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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