Insulin-Like Growth Factor II
Human Recombinant IGF2
Reference ID:KB-2318
Western Blot
Flow Cytometry
Gene of Interest
Gene Synonyms:IGF2;PP1446
Protein Names:Insulin-like growth factor II (IGF-II) (Somatomedin-A) (T3M-11-derived growth factor) [Cleaved into: Insulin-like growth factor II; Insulin-like growth factor II Ala-25 Del; Preptin]
Accession Data
Organism:Homo sapiens (Human)
Mass (kDa):201.40
Length (aa):180
Proteomics (Proteome ID):UP000005640
Proteomics (Chromosome): Chromosome 11
Mass Spectrometry: Mass=7469.4; Method=MALDI; Range=25-91; Evidence={ECO:0000269|PubMed:12586351, ECO:0000269|PubMed:15359740}; Mass=7398.3; Method=MALDI; Range=26-91; Evidence={ECO:0000269|PubMed:12586351, ECO:0000269|PubMed:15359740};
Polymorphism: Genetic variations in IGF2 are associated with body mass index (BMI). The BMI is a statistical measurement which compares a person's weight and height. {ECO:0000269|PubMed:11448941}.
Function [CC]:The insulin-like growth factors possess growth-promoting activity. Major fetal growth hormone in mammals. Plays a key role in regulating fetoplacental development. IGF-II is influenced by placental lactogen. Also involved in tissue differentiation. Positively regulates myogenic transcription factor MYOD1 function by facilitating the recruitment of transcriptional coactivators, thereby controlling muscle terminal differentiation (By similarity). In adults, involved in glucose metabolism in adipose tissue, skeletal muscle and liver (Probable). Acts as a ligand for integrin which is required for IGF2 signaling (PubMed:28873464). {ECO:0000250|UniProtKB:P09535, ECO:0000269|PubMed:28873464, ECO:0000305|PubMed:24593700}.; Preptin undergoes glucose-mediated co-secretion with insulin, and acts as physiological amplifier of glucose-mediated insulin secretion. Exhibits osteogenic properties by increasing osteoblast mitogenic activity through phosphoactivation of MAPK1 and MAPK3. {ECO:0000269|PubMed:16912056}.
Site:SITE 48 48 Important for interaction with integrin. {ECO:0000269|PubMed:28873464}.; SITE 58 58 Important for interaction with integrin. {ECO:0000269|PubMed:28873464}.; SITE 61 61 Important for interaction with integrin. {ECO:0000269|PubMed:28873464}.; SITE 62 62 Important for interaction with integrin. {ECO:0000269|PubMed:28873464}.
Developmental Stage:During embryogenesis, detected in liver, lung, skeletal muscle and placenta. {ECO:0000269|PubMed:16531418}.
Tissue Specificity:Expressed in heart, placenta, lung, liver, muscle, kidney, tongue, limb, eye and pancreas. {ECO:0000269|PubMed:16531418}.
Disease:Silver-Russell syndrome (SRS) [MIM:180860]: A clinically heterogeneous condition characterized by severe intrauterine growth retardation, poor postnatal growth, craniofacial features such as a triangular shaped face and a broad forehead, body asymmetry, and a variety of minor malformations. The phenotypic expression changes during childhood and adolescence, with the facial features and asymmetry usually becoming more subtle with age. {ECO:0000269|PubMed:19066168}. Note=The gene represented in this entry is involved in disease pathogenesis. Most of the cases of Silver-Russell syndrome are caused by the epigenetic changes of DNA hypomethylation at the telomeric imprinting control region (ICR1) on chromosome 11p15, involving the H19 and IGF2 genes.; Growth restriction, severe, with distinctive facies (GRDF) [MIM:616489]: A disease characterized by severe prenatal and postnatal growth restriction, facial dysmorphism, and short stature in the presence of normal or slightly elevated growth hormone levels. {ECO:0000269|PubMed:26154720}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Mutagenesis:MUTAGEN 48 48 R->E: Does not affect integrin binding. Defective integrin binding and IGF2 signaling; when associated with E-58; E-61 and E-62. {ECO:0000269|PubMed:28873464}.; MUTAGEN 58 58 R->E: Does not affect integrin binding. Defective integrin binding and IGF2 signaling; when associated with E-48; E-61 and E-62. {ECO:0000269|PubMed:28873464}.; MUTAGEN 61 61 R->E: Does not affect integrin binding. Defective integrin binding and IGF2 signaling; when associated with E-48; E-58 and E-62. {ECO:0000269|PubMed:28873464}.; MUTAGEN 62 62 R->E: Does not affect integrin binding. Defective integrin binding and IGF2 signaling; when associated with E-48; E-58 and E-61. {ECO:0000269|PubMed:28873464}.; MUTAGEN 64 64 R->E: Slight but significant increase in integrin binding. {ECO:0000269|PubMed:28873464}.; MUTAGEN 92 92 R->A: Decreases mature IGF2 levels. {ECO:0000269|PubMed:16040806}.; MUTAGEN 112 112 K->A: No effect in proteolytical processing. {ECO:0000269|PubMed:16040806}.; MUTAGEN 128 128 R->A: Abolishes proteolytical processing. {ECO:0000269|PubMed:16040806}.
Miscellaneous [CC]:The IGF2 locus is imprinted. Paternal inherited gene is expressed, while the maternal inherited gene is imprinted, hence silenced. Transcripts from 5 promoters P0, P1, P2, P3 and P4 code for the same protein but are differentially regulated in a developmental stage and tissue specificity. {ECO:0000305|PubMed:16531418}.
Reagent Data
Name:Insulin-Like Growth Factor II
Class:Growth Factor
Molecular Weight:7.505
Measured:90-110 IU/mg
Determined By:Assay (Variable)
Assay Profile:LOT-Specific (Check COA)
Formulation:Sterile-filtered colorless solution
Formulation Concentration:1 mg/ml
Buffer Volume:Standard
Buffer Solution:PBS
Endotoxin Level:< 1%
Aggregate Tested By:SDS-PAGE
Endotoxin Screened:< 0.1 ng/ug
Purity:> 97%
Determined: SDS-PAGE
Validated: RP-HPLC
Sample Handling
Stability:This bioreagent is stable at 4°C (short-term) and -70°C(long-term). After reconstitution, sample may be stored at 4°C for 2-7 days and below -18°C for future use.
Preparation:Reconstitute in sterile distilled H2O to no less than 100 ug/ml; dilute reconstituted stock further in other aqueous solutions if needed. Please review COA for lot-specific instructions. Final measurements should be determined by the end-user for optimal performance.