CPNE7
Copine-7
Also known as: CPNE7_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9UBL6
- Gene
- CPNE7
- Ensembl
- ENSG00000178773
- Chromosome
- 16
- Canonical length
- 633 aa
- Protein class
- Metabolic proteins, Predicted intracellular proteins
OverviewNCBI Gene
This gene encodes a member of the copine family, which is composed of calcium-dependent membrane-binding proteins. The gene product contains two N-terminal C2 domains and one von Willebrand factor A domain. The encoded protein may be involved in membrane trafficking. Two alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Nov 2008]
Canonical amino-acid sequenceUniProt
633 residues, UniProt reviewed canonical sequence.
>Q9UBL6|CPNE7
1 MSAGSERGAA ATPGGLPAPC ASKVELRLSC RHLLDRDPLT KSDPSVALLQ QAQGQWVQVG
61 RTEVVRSSLH PVFSKVFTVD YYFEEVQRLR FEVYDTHGPS GFSCQEDDFL GGMECTLGQP
121 AQKWLLQVVM RVSVDVLGPA GHCAKHFLCC TESSHLARTG PSFLLRYDDL CLPWATAGAV
181 RWWTCRGGHT QGWQIVAQKK VTRPLLLKFG RNAGKSTITV IAEDISGNNG YVELSFRARK
241 LDDKDLFSKS DPFLELYRVN DDQGLQLVYR TEVVKNNLNP VWEAFKVSLS SLCSCEETRP
301 LKCLVWDYDS RGKHDFIGEF STTFEEMQKA FEEGQAQWDC VNPKYKQKRR SYKNSGVVVL
361 ADLKFHRVYS FLDYIMGGCQ IHFTVAIDFT ASNGDPRNSC SLHYINPYQP NEYLKALVSV
421 GEICQDYDSD KRFSALGFGA RIPPKYEVSH DFAINFNPED DECEGIQGVV EAYQNCLPRV
481 QLYGPTNVAP IISKVARVAA AEESTGKASQ YYILLILTDG VVTDMADTRE AIVRASRLPM
541 SIIIVGVGNA DFTDMQVLDG DDGVLRSPRG EPALRDIVQF VPFRELKNAS PAALAKCVLA
601 EVPKQVVEYY SHRGLPPRSL GVPAGEASPG CTPLocalizationUniProt · AlphaFold · HPA
Whether an antibody against CPNE7 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
- 0
- Mean surface accessibility (rSASA)
- 0.32
- Highest tissue expression
- 18 nTPM
Expression across tissuesHPA
Tissue
- epididymis: 18 nTPM
- cerebral cortex: 17 nTPM
- hypothalamus: 16 nTPM
- pituitary gland: 13 nTPM
- amygdala: 10 nTPM
- hippocampal formation: 8.8 nTPM
Single-cell type
- epididymal principal cells: 75 nCPM
- innate lymphoid cells: 48 nCPM
- corticotrophs: 39 nCPM
- differentiating spermatogonia: 35 nCPM
- other brain neurons: 24 nCPM
- retinal amacrine cells: 23 nCPM
Immune cell
- MAIT T-cell: 4.9 nTPM
- memory CD8 T-cell: 1.8 nTPM
- memory CD4 T-cell: 1.1 nTPM
- NK-cell: 0.9 nTPM
- gdT-cell: 0.7 nTPM
- T-reg: 0.2 nTPM
Brain region
- thalamus: 62 nTPM
- cerebral cortex: 39 nTPM
- midbrain: 36 nTPM
- amygdala: 31 nTPM
- basal ganglia: 31 nTPM
- hypothalamus: 27 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)
- 1.38
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.98
- DepMap mean gene effect
- -0.19
- 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
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads CPNE7 as an antibody target. Whether an autoantibody or antibody against CPNE7 could matter depends on whether native CPNE7 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CPNE7 is annotated at the cell surface, where native CPNE7 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 CPNE7 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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