Seroatlas · Human Serome Atlas

ACSL4

Long-chain-fatty-acid--CoA ligase 4

Also known as: ACS4, ACSL4_HUMAN, FACL4, LACS4, MRX63, MRX68

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

Protein identityUniProt · HPA

UniProt accession
O60488
Gene
ACSL4
Ensembl
ENSG00000068366
Chromosome
X
Canonical length
711 aa
Protein class
Disease related genes, Enzymes, Human disease related genes, Metabolic proteins, Plasma proteins, Potential drug targets, Predicted intracellular proteins, Predicted membrane proteins
Subcellular location
Golgi apparatus,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 preferentially utilizes arachidonate as substrate. The absence of this enzyme may contribute to the cognitive disability or Alport syndrome. Alternative splicing of this gene generates multiple transcript variants. [provided by RefSeq, Jan 2016]

Canonical amino-acid sequenceUniProt

711 residues, UniProt reviewed canonical sequence.

>O60488|ACSL4
     1  MKLKLNVLTI ILLPVHLLIT IYSALIFIPW YFLTNAKKKN AMAKRIKAKP TSDKPGSPYR
    61  SVTHFDSLAV IDIPGADTLD KLFDHAVSKF GKKDSLGTRE ILSEENEMQP NGKVFKKLIL
   121  GNYKWMNYLE VNRRVNNFGS GLTALGLKPK NTIAIFCETR AEWMIAAQTC FKYNFPLVTL
   181  YATLGKEAVV HGLNESEASY LITSVELLES KLKTALLDIS CVKHIIYVDN KAINKAEYPE
   241  GFEIHSMQSV EELGSNPENL GIPPSRPTPS DMAIVMYTSG STGRPKGVMM HHSNLIAGMT
   301  GQCERIPGLG PKDTYIGYLP LAHVLELTAE ISCFTYGCRI GYSSPLTLSD QSSKIKKGSK
   361  GDCTVLKPTL MAAVPEIMDR IYKNVMSKVQ EMNYIQKTLF KIGYDYKLEQ IKKGYDAPLC
   421  NLLLFKKVKA LLGGNVRMML SGGAPLSPQT HRFMNVCFCC PIGQGYGLTE SCGAGTVTEV
   481  TDYTTGRVGA PLICCEIKLK DWQEGGYTIN DKPNPRGEIV IGGQNISMGY FKNEEKTAED
   541  YSVDENGQRW FCTGDIGEFH PDGCLQIIDR KKDLVKLQAG EYVSLGKVEA ALKNCPLIDN
   601  ICAFAKSDQS YVISFVVPNQ KRLTLLAQQK GVEGTWVDIC NNPAMEAEIL KEIREAANAM
   661  KLERFEIPIK VRLSPEPWTP ETGLVTDAFK LKRKELRNHY LKDIERMYGG K

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against ACSL4 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
62 nTPM

Expression across tissuesHPA

Tissue

  • urinary bladder: 62 nTPM
  • cervix: 44 nTPM
  • kidney: 42 nTPM
  • skeletal muscle: 39 nTPM
  • adipose tissue: 38 nTPM
  • lung: 35 nTPM

Single-cell type

  • neutrophils: 1,708 nCPM
  • mast cells: 1,267 nCPM
  • distal convoluted tubule cells: 905 nCPM
  • epicardial cells: 459 nCPM
  • sertoli cells: 453 nCPM
  • alveolar cells type 2: 427 nCPM

Immune cell

  • eosinophil: 35 nTPM
  • basophil: 31 nTPM
  • neutrophil: 30 nTPM
  • non-classical monocyte: 20 nTPM
  • intermediate monocyte: 16 nTPM
  • classical monocyte: 11 nTPM

Brain region

  • hypothalamus: 55 nTPM
  • pons: 50 nTPM
  • cerebral cortex: 47 nTPM
  • midbrain: 45 nTPM
  • hippocampal formation: 41 nTPM
  • thalamus: 41 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about ACSL4.

Disease | AllUniProt

Conditions ACSL4 is implicated in, by any mechanism.

  • Intellectual developmental disorder, X-linked 63 (XLID63) MIM:300387
  • AMME complex (ATS-MR) MIM:300194

Disease | GeneticClinVar

14 pathogenic / likely-pathogenic of 342 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

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)
0.31
gnomAD pLI
0.98
gnomAD missense Z
2.59
DepMap mean gene effect
-0.18
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 ACSL4 as an antibody target. Whether an autoantibody or antibody against ACSL4 could matter depends on whether native ACSL4 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

ACSL4 is annotated at the cell surface, where native ACSL4 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 ACSL4 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/ACSL4. 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).

© 2026 · Seroatlas, Discover Oregon LLC · Terms of use

Loading the interactive Seroatlas protein explorer...