ACAA1
3-ketoacyl-CoA thiolase, peroxisomal
Also known as: Lnc-Myd88, THIK_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P09110
- Gene
- ACAA1
- Ensembl
- ENSG00000060971
- Chromosome
- 3
- Canonical length
- 424 aa
- Protein class
- Enzymes, Metabolic proteins, Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Peroxisomes
- Quaternary structure
- Homodimer
OverviewNCBI Gene
This gene encodes an enzyme operative in the beta-oxidation system of the peroxisomes. Deficiency of this enzyme leads to pseudo-Zellweger syndrome. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
424 residues, UniProt reviewed canonical sequence.
>P09110|ACAA1
1 MQRLQVVLGH LRGPADSGWM PQAAPCLSGA PQASAADVVV VHGRRTAICR AGRGGFKDTT
61 PDELLSAVMT AVLKDVNLRP EQLGDICVGN VLQPGAGAIM ARIAQFLSDI PETVPLSTVN
121 RQCSSGLQAV ASIAGGIRNG SYDIGMACGV ESMSLADRGN PGNITSRLME KEKARDCLIP
181 MGITSENVAE RFGISREKQD TFALASQQKA ARAQSKGCFQ AEIVPVTTTV HDDKGTKRSI
241 TVTQDEGIRP STTMEGLAKL KPAFKKDGST TAGNSSQVSD GAAAILLARR SKAEELGLPI
301 LGVLRSYAVV GVPPDIMGIG PAYAIPVALQ KAGLTVSDVD IFEINEAFAS QAAYCVEKLR
361 LPPEKVNPLG GAVALGHPLG CTGARQVITL LNELKRRGKR AYGVVSMCIG TGMGAAAVFE
421 YPGNLocalizationUniProt · AlphaFold · HPA
Whether an antibody against ACAA1 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
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.25
- Highest tissue expression
- 616 nTPM
Expression across tissuesHPA
Tissue
- liver: 616 nTPM
- kidney: 198 nTPM
- duodenum: 95 nTPM
- small intestine: 84 nTPM
- heart muscle: 79 nTPM
- midbrain: 63 nTPM
Single-cell type
- hepatocytes: 841 nCPM
- esophageal apical cells: 450 nCPM
- enterocytes: 408 nCPM
- colonocytes: 311 nCPM
- esophageal suprabasal cells: 153 nCPM
- urothelial cells: 144 nCPM
Immune cell
- non-classical monocyte: 189 nTPM
- myeloid DC: 178 nTPM
- intermediate monocyte: 159 nTPM
- eosinophil: 131 nTPM
- classical monocyte: 115 nTPM
- plasmacytoid DC: 105 nTPM
Brain region
- white matter: 52 nTPM
- cerebellum: 52 nTPM
- medulla oblongata: 52 nTPM
- thalamus: 52 nTPM
- basal ganglia: 52 nTPM
- spinal cord: 46 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)
- 1.12
- gnomAD pLI
- 0
- gnomAD missense Z
- 1.22
- DepMap mean gene effect
- 0.13
- 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
- alpha-linolenic acid metabolic process
- bile acid metabolic process
- fatty acid beta-oxidation
- fatty acid beta-oxidation using acyl-CoA oxidase
- very long-chain fatty acid metabolic process
- phenylacetate catabolic process
Molecular functions
- acetyl-CoA C-acetyltransferase activity
- acetyl-CoA C-acyltransferase activity
- acetyl-CoA C-myristoyltransferase activity
- long-chain fatty acyl-CoA oxidase activity
- acetate CoA-transferase activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads ACAA1 as an antibody target. Whether an autoantibody or antibody against ACAA1 could matter depends on whether native ACAA1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
ACAA1 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 ACAA1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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