SULT1A4
Sulfotransferase 1A4
Also known as: ST1A4_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P0DMN0
- Gene
- SULT1A4
- Ensembl
- ENSG00000213648
- Chromosome
- 16
- Canonical length
- 295 aa
- Protein class
- Enzymes, Metabolic proteins, Predicted intracellular proteins
- Quaternary structure
- Homodimer
OverviewNCBI Gene
Sulfotransferase enzymes catalyze the sulfate conjugation of many hormones, neurotransmitters, drugs, and xenobiotic compounds. These cytosolic enzymes are different in their tissue distributions and substrate specificities. The gene structure (number and length of exons) is similar among family members. This gene encodes a phenol sulfotransferase with thermolabile enzyme activity. Four sulfotransferase genes are located on the p arm of chromosome 16, this gene and SULT1A3 arose from a segmental duplication. Read-through transcription exists between this gene and the upstream SLX1B (SLX1 structure-specific endonuclease subunit homolog B) gene that encodes a protein containing GIY-YIG domains. [provided by RefSeq, Nov 2010]
Canonical amino-acid sequenceUniProt
295 residues, UniProt reviewed canonical sequence.
>P0DMN0|SULT1A4
1 MELIQDTSRP PLEYVKGVPL IKYFAEALGP LQSFQARPDD LLINTYPKSG TTWVSQILDM
61 IYQGGDLEKC NRAPIYVRVP FLEVNDPGEP SGLETLKDTP PPRLIKSHLP LALLPQTLLD
121 QKVKVVYVAR NPKDVAVSYY HFHRMEKAHP EPGTWDSFLE KFMAGEVSYG SWYQHVQEWW
181 ELSRTHPVLY LFYEDMKENP KREIQKILEF VGRSLPEETM DFMVQHTSFK EMKKNPMTNY
241 TTVPQELMDH SISPFMRKGM AGDWKTTFTV AQNERFDADY AEKMAGCSLS FRSELLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SULT1A4 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)
- 0.23
- Highest tissue expression
- 27 nTPM
Expression across tissuesHPA
Tissue
- duodenum: 27 nTPM
- small intestine: 27 nTPM
- colon: 8.4 nTPM
- heart muscle: 7.8 nTPM
- rectum: 7.1 nTPM
- spleen: 7 nTPM
Single-cell type
- colonocytes: 0.6 nCPM
- endometrial secretory cells: 0.3 nCPM
- distal convoluted tubule cells: 0.2 nCPM
- enteric stem cells: 0.2 nCPM
- enteric transient amplifying cells: 0.2 nCPM
- goblet cells: 0.2 nCPM
Immune cell
- intermediate monocyte: 25 nTPM
- myeloid DC: 18 nTPM
- classical monocyte: 7.2 nTPM
- non-classical monocyte: 5.6 nTPM
- total PBMC: 5.4 nTPM
- basophil: 1.9 nTPM
Brain region
- medulla oblongata: 5.8 nTPM
- cerebral cortex: 5.7 nTPM
- hypothalamus: 5 nTPM
- pons: 4.5 nTPM
- white matter: 4.4 nTPM
- cerebellum: 4.2 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)
- 1.74
- gnomAD pLI
- 0.38
- gnomAD missense Z
- 0.98
OntologyGO
Biological processes
- dopamine metabolic process
- epinephrine metabolic process
- norepinephrine metabolic process
- serotonin metabolic process
- steroid metabolic process
- sulfation
- thyroid hormone metabolic process
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads SULT1A4 as an antibody target. Whether an autoantibody or antibody against SULT1A4 could matter depends on whether native SULT1A4 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SULT1A4 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 SULT1A4 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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