SVIP
Small VCP/p97-interacting protein
Also known as: DKFZp313A2432, SVIP_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q8NHG7
- Gene
- SVIP
- Ensembl
- ENSG00000198168
- Chromosome
- 11
- Canonical length
- 77 aa
- Protein class
- Predicted intracellular proteins
OverviewNCBI Gene
Endoplasmic reticulum-associated degradation (ERAD) is the pathway by which misfolded proteins in the endoplasmic reticulum are targeted to the proteasome for degradation. Multiple specialized proteins interact with one another during ERAD to complete this process. The protein encoded by this gene is an inhibitor of ERAD, functioning to disrupt the interaction of these protein components. This downregulation of ERAD may be needed to protect the cell from overactive protein degradation. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Feb 2016]
Canonical amino-acid sequenceUniProt
77 residues, UniProt reviewed canonical sequence.
>Q8NHG7|SVIP
1 MGLCFPCPGE SAPPTPDLEE KRAKLAEAAE RRQKEAASRG ILDVQSVQEK RKKKEKIEKQ
61 IATSGPPPEG GLRWTVSLocalizationUniProt · AlphaFold · HPA
Whether an antibody against SVIP 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)
- 0.58
- Highest tissue expression
- 28 nTPM
Expression across tissuesHPA
Tissue
- spinal cord: 28 nTPM
- thyroid gland: 22 nTPM
- stomach: 18 nTPM
- epididymis: 17 nTPM
- bone marrow: 17 nTPM
- hypothalamus: 16 nTPM
Single-cell type
- early spermatids: 1,014 nCPM
- platelets: 911 nCPM
- late primary spermatocytes: 752 nCPM
- parietal cells: 453 nCPM
- oocytes: 387 nCPM
- late spermatids: 386 nCPM
Immune cell
- plasmacytoid DC: 24 nTPM
- eosinophil: 23 nTPM
- naive CD4 T-cell: 16 nTPM
- memory CD4 T-cell: 13 nTPM
- memory B-cell: 13 nTPM
- naive B-cell: 13 nTPM
Brain region
- white matter: 31 nTPM
- spinal cord: 27 nTPM
- medulla oblongata: 24 nTPM
- hypothalamus: 24 nTPM
- thalamus: 24 nTPM
- pons: 24 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)
- 1.85
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.44
- DepMap mean gene effect
- 0.01
- DepMap dependency class
- none
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
- negative regulation of ERAD pathway
- negative regulation of protein-containing complex assembly
- negative regulation of retrograde protein transport, ER to cytosol
- positive regulation of autophagy
- positive regulation of protein lipidation
- negative regulation of VCP-NPL4-UFD1 AAA ATPase complex assembly
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Small VCP/p97-interacting protein
- Small VCP/p97-interacting protein, metazoa
- Small VCP/p97-interacting protein
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of SVIP 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 SVIP as an antibody target. Whether an autoantibody or antibody against SVIP could matter depends on whether native SVIP is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
SVIP is annotated at the cell surface, where native SVIP 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 SVIP as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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