INS-IGF2

Protein identityUniProt · HPA

UniProt accession

F8WCM5

Gene

INS-IGF2

Ensembl

ENSG00000129965

Chromosome

11

Canonical length

200 aa

Protein class

Predicted secreted proteins

Subcellular location

Nucleoplasm

Secretome location

Secreted to digestive system

OverviewNCBI Gene

This locus includes two alternatively spliced read-through transcript variants which align to the INS gene in the 5' region and to the IGF2 gene in the 3' region. One transcript is predicted to encode a protein which shares the N-terminus with the INS protein but has a distinct and longer C-terminus, whereas the other transcript is a candidate for nonsense-mediated decay (NMD). The transcripts are imprinted and are paternally expressed in the limb and eye. [provided by RefSeq, Jul 2008]

Canonical amino-acid sequenceUniProt

200 residues, UniProt reviewed canonical sequence.

>F8WCM5|INS-IGF2
     1  MALWMRLLPL LALLALWGPD PAAAFVNQHL CGSHLVEALY LVCGERGFFY TPKTRREAED
    61  LQASALSLSS STSTWPEGLD ATARAPPALV VTANIGQAGG SSSRQFRQRA LGTSDSPVLF
   121  IHCPGAAGTA QGLEYRGRRV TTELVWEEVD SSPQPQGSES LPAQPPAQPA PQPEPQQARE
   181  PSPEVSCCGL WPRRPQRSQN

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against INS-IGF2 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

Secreted

Secreted

Yes

Transmembrane segments

0

Mean surface accessibility (rSASA)

0.68

Highest tissue expression

8.3 nTPM

Expression across tissuesHPA

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about INS-IGF2.

Disease | GeneticClinVar

1 pathogenic / likely-pathogenic of 28 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

• Maturity-onset diabetes of the young type 10

Disease | ImmuneIEDB

Conditions an epitope on INS-IGF2 was assayed in.

• type 1 diabetes mellitus T cell

ReferencesPubMed · IEDB

Publications for INS-IGF2 from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.

Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. IEDB — curated epitope assays from the Immune Epitope Database (Vita et al., Nucleic Acids Research 2019). Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.

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)

1.04

gnomAD pLI

0.06

gnomAD missense Z

0.01

OntologyGO

Molecular functions

• hormone activity
• insulin receptor binding

Cellular components

• extracellular space

Protein domainsUniProt · Pfam · InterPro

• Insulin-like
• Insulin-like superfamily
• Insulin/IGF/Relaxin family
• Insulin