INSIG2
Insulin-induced gene 2 protein
Also known as: INSI2_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9Y5U4
- Gene
- INSIG2
- Ensembl
- ENSG00000125629
- Chromosome
- 2
- Canonical length
- 225 aa
- Protein class
- Predicted membrane proteins, Transporters
OverviewNCBI Gene
The protein encoded by this gene is highly similar to the protein product encoded by gene INSIG1. Both INSIG1 protein and this protein are endoplasmic reticulum proteins that block the processing of sterol regulatory element binding proteins (SREBPs) by binding to SREBP cleavage-activating protein (SCAP), and thus prevent SCAP from escorting SREBPs to the Golgi. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
225 residues, UniProt reviewed canonical sequence.
>Q9Y5U4|INSIG2
1 MAEGETESPG PKKCGPYISS VTSQSVNLMI RGVVLFFIGV FLALVLNLLQ IQRNVTLFPP
61 DVIASIFSSA WWVPPCCGTA SAVIGLLYPC IDRHLGEPHK FKREWSSVMR CVAVFVGINH
121 ASAKVDFDNN IQLSLTLAAL SIGLWWTFDR SRSGFGLGVG IAFLATVVTQ LLVYNGVYQY
181 TSPDFLYVRS WLPCIFFAGG ITMGNIGRQL AMYECKVIAE KSHQELocalizationUniProt · AlphaFold · HPA
Whether an antibody against INSIG2 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
- 6
- Mean surface accessibility (rSASA)
- 0.35
- Highest tissue expression
- 21 nTPM
Expression across tissuesHPA
Tissue
- liver: 21 nTPM
- parathyroid gland: 9.8 nTPM
- kidney: 9.3 nTPM
- spleen: 8.6 nTPM
- cerebral cortex: 8 nTPM
- blood vessel: 7.9 nTPM
Single-cell type
- pancreatic duct cells: 135 nCPM
- pancreatic acinar cells: 126 nCPM
- esophageal apical cells: 109 nCPM
- gastric chief cells: 89 nCPM
- alveolar cells type 1: 84 nCPM
- parietal cells: 81 nCPM
Immune cell
- eosinophil: 7.7 nTPM
- non-classical monocyte: 7.4 nTPM
- intermediate monocyte: 6 nTPM
- naive CD8 T-cell: 5.9 nTPM
- NK-cell: 5.9 nTPM
- naive CD4 T-cell: 5.3 nTPM
Brain region
- cerebellum: 16 nTPM
- hippocampal formation: 15 nTPM
- choroid plexus: 14 nTPM
- thalamus: 14 nTPM
- cerebral cortex: 14 nTPM
- midbrain: 13 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)
- 0.77
- gnomAD pLI
- 0.06
- gnomAD missense Z
- 1.84
- DepMap mean gene effect
- 0.01
- 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 response to insulin stimulus
- cholesterol biosynthetic process
- cranial suture morphogenesis
- inner ear morphogenesis
- middle ear morphogenesis
- negative regulation of fatty acid biosynthetic process
- negative regulation of steroid biosynthetic process
- response to fatty acid
- roof of mouth development
- SREBP signaling pathway
- SREBP-SCAP complex retention in endoplasmic reticulum
- triglyceride metabolic process
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of INSIG2 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 INSIG2 as an antibody target. Whether an autoantibody or antibody against INSIG2 could matter depends on whether native INSIG2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
INSIG2 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 INSIG2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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