NTAQ1
Protein N-terminal glutamine amidohydrolase
Also known as: C8orf32, FLJ10204, NTAQ1_HUMAN, WDYHV1
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q96HA8
- Gene
- NTAQ1
- Ensembl
- ENSG00000156795
- Chromosome
- 8
- Canonical length
- 205 aa
- Protein class
- Enzymes, Metabolic proteins, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Vesicles
OverviewNCBI Gene
Predicted to enable protein-N-terminal glutamine amidohydrolase activity. Predicted to be involved in protein modification process. Predicted to be located in cytoplasm. Predicted to be active in cytosol and nucleus. [provided by Alliance of Genome Resources, Apr 2025]
Canonical amino-acid sequenceUniProt
205 residues, UniProt reviewed canonical sequence.
>Q96HA8|NTAQ1
1 MEGNGPAAVH YQPASPPRDA CVYSSCYCEE NIWKLCEYIK NHDQYPLEEC YAVFISNERK
61 MIPIWKQQAR PGDGPVIWDY HVVLLHVSSG GQNFIYDLDT VLPFPCLFDT YVEDAFKSDD
121 DIHPQFRRKF RVIRADSYLK NFASDRSHMK DSSGNWREPP PPYPCIETGD SKMNLNDFIS
181 MDPKVGWGAV YTLSEFTHRF GSKNCLocalizationUniProt · AlphaFold · HPA
Whether an antibody against NTAQ1 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)
- 0.29
- Highest tissue expression
- 20 nTPM
Expression across tissuesHPA
Tissue
- skeletal muscle: 20 nTPM
- choroid plexus: 20 nTPM
- hypothalamus: 20 nTPM
- heart muscle: 19 nTPM
- ovary: 19 nTPM
- spinal cord: 18 nTPM
Single-cell type
- differentiating spermatogonia: 56 nCPM
- retinal horizontal cells: 40 nCPM
- sertoli cells: 39 nCPM
- undifferentiated spermatogonia: 39 nCPM
- oocytes: 37 nCPM
- gastric progenitor cells: 36 nCPM
Immune cell
- basophil: 16 nTPM
- NK-cell: 16 nTPM
- T-reg: 11 nTPM
- myeloid DC: 9.1 nTPM
- intermediate monocyte: 8.7 nTPM
- memory CD8 T-cell: 7.7 nTPM
Brain region
- thalamus: 24 nTPM
- hypothalamus: 21 nTPM
- midbrain: 19 nTPM
- white matter: 18 nTPM
- pons: 18 nTPM
- medulla oblongata: 18 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)
- 1.35
- gnomAD pLI
- 0
- DepMap mean gene effect
- 0.1
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 14% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
Molecular functions
- protein-N-terminal asparagine amidohydrolase activity
- protein-N-terminal glutamine amidohydrolase activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Protein N-terminal glutamine amidohydrolase, alpha beta roll
- Protein N-terminal glutamine amidohydrolase, alpha beta roll superfamily
- Protein N-terminal glutamine amidohydrolase
- N-terminal glutamine amidase
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of NTAQ1 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads NTAQ1 as an antibody target. Whether an autoantibody or antibody against NTAQ1 could matter depends on whether native NTAQ1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
NTAQ1 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 NTAQ1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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