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proteins. Page last changed on 25 Jan 2016.
Insulin-like growth factor 2
Insulin-Like Growth Factor II, IGF-II, IGF2
This gene encodes a member of the insulin family of polypeptide growth factors, which are involved in development and growth. It is an imprinted gene, expressed only from the paternal allele, and epigenetic changes at this locus are associated with Wilms tumour, Beckwith-Wiedemann syndrome, rhabdomyosarcoma, and Silver-Russell syndrome. A read-through INS-IGF2 gene exists, whose 5' region overlaps the INS gene and the 3' region overlaps this gene. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2010] (from
Maehara et al., Fukuoka, Japan. In Liver Transpl, 19 Feb 2016
In HCC cells, miR-18a regulated the expression of tumor necrosis factor alpha induced protein 3 (TNFAIP3), and miR-199a-5p regulated the expression of hypoxia-inducible factor 1 alpha (HIF1A), vascular endothelial growth factor A (VEGFA), insulin-like growth factor 1 receptor (IGF1R), and insulin-like growth factor 2 (IGF2).
Ligato et al., Hartford, United States. In Appl Immunohistochem Mol Morphol, 13 Feb 2016
CONTEXT: α-methylacyl coenzyme A racemase (AMACR) and insulin-like growth factor-II mRNA-binding protein 3 (IMP3) are 2 markers helpful in detecting difficult cases of dysplasia in Barrett esophagus (BE).
In this retrospective case control study we examined the association between small for gestational age children (SGA) and both DNA methylation and gene expression levels of the genes WNT2, IGF2/H19, SERPINA3, HERVWE1 and PPARG in first trimester placental tissue.
Drake et al., Edinburgh, United Kingdom. In Lancet, Mar 2015
We hypothesised that preterm infants have altered 5mC at the linked differentially methylated region 2 (DMR2) of IGF2 and the H19 imprinting control region (H19 ICR) compared with term infants over the first year of life.
Gessler et al., Würzburg, Germany. In Cancer Cell, Mar 2015
Recurrent mutations included a hotspot mutation (Q177R) in the homeo-domain of SIX1 and SIX2 in tumors with high proliferative potential (18.1% of blastemal cases); mutations in the DROSHA/DGCR8 microprocessor genes (18.2% of blastemal cases); mutations in DICER1 and DIS3L2; and alterations in IGF2, MYCN, and TP53, the latter being strongly associated with dismal outcome.
significant IGF2 hypermethylation (20 +/- 10 vs. 14 +/- 7%; p<0.05) and SNURF hypomethylation (23 +/- 6 vs. 32 6%; p<0.001) was found in Albright's hereditary osteodystrophy patients vs. controls.