Seroatlas · Human Serome Atlas

NMES1

Normal mucosa of esophagus-specific gene 1 protein

Also known as: C15orf48, COXFA4L3, MIR147BHG, MISTRAV, MOCCI, NMES1_HUMAN

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

Protein identityUniProt · HPA

UniProt accession
Q9C002
Gene
NMES1
Ensembl
ENSG00000166920
Chromosome
15
Canonical length
83 aa
Protein class
Predicted intracellular proteins

OverviewNCBI Gene

This gene was first identified in a study of human esophageal squamous cell carcinoma tissues. Levels of both the message and protein are reduced in carcinoma samples. In adult human tissues, this gene is expressed in the the esophagus, stomach, small intestine, colon and placenta. Alternatively spliced transcript variants that encode the same protein have been identified. [provided by RefSeq, Jun 2012]

Canonical amino-acid sequenceUniProt

83 residues, UniProt reviewed canonical sequence.

>Q9C002|NMES1
     1  MSFFQLLMKR KELIPLVVFM TVAAGGASSF AVYSLWKTDV ILDRKKNPEP WETVDPTVPQ
    61  KLITINQQWK PIEELQNVQR VTK

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against NMES1 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
Other membrane
Secreted
No
Transmembrane segments
1
Mean surface accessibility (rSASA)
0.48
Highest tissue expression
867 nTPM

Expression across tissuesHPA

Tissue

  • rectum: 867 nTPM
  • colon: 808 nTPM
  • small intestine: 321 nTPM
  • esophagus: 162 nTPM
  • testis: 120 nTPM
  • stomach: 101 nTPM

Single-cell type

  • esophageal apical cells: 5,881 nCPM
  • colonocytes: 3,918 nCPM
  • enterocytes: 2,604 nCPM
  • enteric transient amplifying cells: 2,389 nCPM
  • goblet cells: 1,330 nCPM
  • enteric stem cells: 1,313 nCPM

Immune cell

  • intermediate monocyte: 1.6 nTPM
  • classical monocyte: 1.3 nTPM
  • myeloid DC: 1.3 nTPM
  • neutrophil: 0.8 nTPM
  • total PBMC: 0.8 nTPM
  • non-classical monocyte: 0.2 nTPM

Brain region

  • cerebral cortex: 6.3 nTPM
  • pons: 2.2 nTPM
  • thalamus: 1.8 nTPM
  • choroid plexus: 0.9 nTPM
  • white matter: 0.8 nTPM
  • medulla oblongata: 0.7 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)
1.86
gnomAD pLI
0
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

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads NMES1 as an antibody target. Whether an autoantibody or antibody against NMES1 could matter depends on whether native NMES1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

NMES1 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 NMES1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/NMES1. 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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