TMEM182
Transmembrane protein 182
Also known as: FLJ30294, TM182_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q6ZP80
- Gene
- TMEM182
- Ensembl
- ENSG00000170417
- Chromosome
- 2
- Canonical length
- 229 aa
- Protein class
- Predicted intracellular proteins, Predicted membrane proteins
- Subcellular location
- Nucleoplasm,Vesicles
OverviewNCBI Gene
Predicted to be involved in myotube cell development involved in skeletal muscle regeneration; negative regulation of myoblast differentiation; and negative regulation of myoblast fusion. Predicted to be located in plasma membrane. [provided by Alliance of Genome Resources, Jul 2025]
Canonical amino-acid sequenceUniProt
229 residues, UniProt reviewed canonical sequence.
>Q6ZP80|TMEM182
1 MRLNIAIFFG ALFGALGVLL FLVAFGSDYW LLATEVGRCS GEKNIENVTF HHEGFFWRCW
61 FNGIVEENDS NIWKFWYTNQ PPSKNCTHAY LSPYPFMRGE HNSTSYDSAV IYRGFWAVLM
121 LLGVVAVVIA SFLIICAAPF ASHFLYKAGG GSYIAAGILF SLVVMLYVIW VQAVADMESY
181 RNMKMKDCLD FTPSVLYGWS FFLAPAGIFF SLLAGLLFLV VGWHIQIHHLocalizationUniProt · AlphaFold · HPA
Whether an antibody against TMEM182 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
- 3
- Mean surface accessibility (rSASA)
- 0.29
- Highest tissue expression
- 141 nTPM
Expression across tissuesHPA
Tissue
- skeletal muscle: 141 nTPM
- tongue: 119 nTPM
- heart muscle: 91 nTPM
- epididymis: 5 nTPM
- prostate: 3.8 nTPM
- esophagus: 3.7 nTPM
Single-cell type
- cardiomyocytes: 239 nCPM
- myonuclei: 234 nCPM
- breast lactating cells: 140 nCPM
- early spermatids: 118 nCPM
- thymic myoid cells: 80 nCPM
- hematopoietic stem cells: 62 nCPM
Immune cell
- memory B-cell: 3.6 nTPM
- MAIT T-cell: 2.9 nTPM
- plasmacytoid DC: 2.9 nTPM
- gdT-cell: 2.5 nTPM
- naive CD4 T-cell: 2.4 nTPM
- naive CD8 T-cell: 2.4 nTPM
Brain region
- hypothalamus: 4.5 nTPM
- pons: 4.1 nTPM
- medulla oblongata: 3.7 nTPM
- cerebral cortex: 3.6 nTPM
- midbrain: 3.5 nTPM
- white matter: 3.5 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)
- 0.79
- gnomAD pLI
- 0.06
- gnomAD missense Z
- 0.09
- DepMap mean gene effect
- 0.04
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- muscle organ development
- myotube differentiation involved in skeletal muscle regeneration
- negative regulation of myoblast differentiation
- negative regulation of myoblast fusion
- myotube cell development involved in skeletal muscle regeneration
Cellular components
Protein domainsUniProt · Pfam · InterPro
- PMP-22/EMP/MP20/Claudin
- PMP-22/EMP/MP20/Claudin tight junction
- Transmembrane protein 182
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of TMEM182 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 TMEM182 as an antibody target. Whether an autoantibody or antibody against TMEM182 could matter depends on whether native TMEM182 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
TMEM182 is annotated at the cell surface, where native TMEM182 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 TMEM182 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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