Seroatlas · Human Serome Atlas

ACSL5

Long-chain-fatty-acid--CoA ligase 5

Also known as: ACS2, ACS5, ACSL5_HUMAN, FACL5

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

Protein identityUniProt · HPA

UniProt accession
Q9ULC5
Gene
ACSL5
Ensembl
ENSG00000197142
Chromosome
10
Canonical length
683 aa
Protein class
Enzymes, Metabolic proteins, Plasma proteins, Predicted membrane proteins
Subcellular location
Nucleoplasm,Mitochondria

OverviewNCBI Gene

The protein encoded by this gene is an isozyme of the long-chain fatty-acid-coenzyme A ligase family. Although differing in substrate specificity, subcellular localization, and tissue distribution, all isozymes of this family convert free long-chain fatty acids into fatty acyl-CoA esters, and thereby play a key role in lipid biosynthesis and fatty acid degradation. This isozyme is highly expressed in uterus and spleen, and in trace amounts in normal brain, but has markedly increased levels in malignant gliomas. This gene functions in mediating fatty acid-induced glioma cell growth. Three transcript variants encoding two different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

Canonical amino-acid sequenceUniProt

683 residues, UniProt reviewed canonical sequence.

>Q9ULC5|ACSL5
     1  MLFIFNFLFS PLPTPALICI LTFGAAIFLW LITRPQPVLP LLDLNNQSVG IEGGARKGVS
    61  QKNNDLTSCC FSDAKTMYEV FQRGLAVSDN GPCLGYRKPN QPYRWLSYKQ VSDRAEYLGS
   121  CLLHKGYKSS PDQFVGIFAQ NRPEWIISEL ACYTYSMVAV PLYDTLGPEA IVHIVNKADI
   181  AMVICDTPQK ALVLIGNVEK GFTPSLKVII LMDPFDDDLK QRGEKSGIEI LSLYDAENLG
   241  KEHFRKPVPP SPEDLSVICF TSGTTGDPKG AMITHQNIVS NAAAFLKCVE HAYEPTPDDV
   301  AISYLPLAHM FERIVQAVVY SCGARVGFFQ GDIRLLADDM KTLKPTLFPA VPRLLNRIYD
   361  KVQNEAKTPL KKFLLKLAVS SKFKELQKGI IRHDSFWDKL IFAKIQDSLG GRVRVIVTGA
   421  APMSTSVMTF FRAAMGCQVY EAYGQTECTG GCTFTLPGDW TSGHVGVPLA CNYVKLEDVA
   481  DMNYFTVNNE GEVCIKGTNV FKGYLKDPEK TQEALDSDGW LHTGDIGRWL PNGTLKIIDR
   541  KKNIFKLAQG EYIAPEKIEN IYNRSQPVLQ IFVHGESLRS SLVGVVVPDT DVLPSFAAKL
   601  GVKGSFEELC QNQVVREAIL EDLQKIGKES GLKTFEQVKA IFLHPEPFSI ENGLLTPTLK
   661  AKRGELSKYF RTQIDSLYEH IQD

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against ACSL5 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)
0.23
Highest tissue expression
406 nTPM

Expression across tissuesHPA

Tissue

  • small intestine: 406 nTPM
  • duodenum: 348 nTPM
  • epididymis: 212 nTPM
  • liver: 160 nTPM
  • rectum: 112 nTPM
  • colon: 107 nTPM

Single-cell type

  • enterocytes: 944 nCPM
  • endometrial glandular cells: 607 nCPM
  • urothelial cells: 450 nCPM
  • epididymal principal cells: 280 nCPM
  • endometrial luminal cells: 265 nCPM
  • colonocytes: 207 nCPM

Immune cell

  • T-reg: 44 nTPM
  • myeloid DC: 33 nTPM
  • intermediate monocyte: 30 nTPM
  • memory CD8 T-cell: 30 nTPM
  • non-classical monocyte: 29 nTPM
  • basophil: 29 nTPM

Brain region

  • thalamus: 15 nTPM
  • pons: 14 nTPM
  • cerebral cortex: 12 nTPM
  • medulla oblongata: 12 nTPM
  • spinal cord: 12 nTPM
  • hypothalamus: 11 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about ACSL5.

Disease | AllUniProt

Conditions ACSL5 is implicated in, by any mechanism.

Disease | GeneticClinVar

1 pathogenic / likely-pathogenic of 119 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

  • Diarrhea 13

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)
0.73
gnomAD pLI
0
gnomAD missense Z
0.72
DepMap mean gene effect
0.02
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 ACSL5 as an antibody target. Whether an autoantibody or antibody against ACSL5 could matter depends on whether native ACSL5 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

ACSL5 is annotated at the cell surface, where native ACSL5 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 ACSL5 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/ACSL5. 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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