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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 NCBI)
Top mentioned proteins: Insulin, CAN, Insulin-Like Growth Factor I, HAD, IGF-I receptor
Papers using Insulin-Like Growth Factor II antibodies
LYVE-1, the lymphatic system and tumor lymphangiogenesis
Lahm Harald et al., In Journal of Carcinogenesis, 2000
... Identification of PEPCK-IGF-II transgenic animals and carcinogen treatment ...
Papers on Insulin-Like Growth Factor II
Genomic insights into growth and its disorders: an update.
Dauber et al., Cincinnati, United States. In Curr Opin Endocrinol Diabetes Obes, Feb 2016
Several new developments in imprinted growth-related genes (including the first human mutation in insulin-like growth factor II) and novel insights into the epigenetic regulation of growth have been reported.
Proteomic analysis of the INS-1E secretome identify novel vitamin D-regulated proteins.
Thorsby et al., Oslo, Norway. In Diabetes Metab Res Rev, Feb 2016
Up-regulation of proteins implicated in β-cell growth and proliferation, such as IGF2, IGFBP7 and gelsolin, suggest that 1,25-(OH)2 D3 has a positive effect on β-cell growth and proliferation.
Relevance of MicroRNA-18a and MicroRNA-199a-5p to hepatocellular carcinoma recurrence after living donor liver transplantation.
Maehara et al., Fukuoka, Japan. In Liver Transpl, 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).
Mastermind-like 3 controls proliferation and differentiation in neuroblastoma.
Bajpe et al., Netherlands. In Mol Cancer Res, Feb 2016
Additionally, MAML3 has RA-independent functions, including the activation of IGF1R and downstream AKT signaling via upregulation of IGF2, resulting in increased proliferation.
TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.
Mishra et al., In J Clin Invest, Feb 2016
Moreover, tumorigenesis-associated genes IGF2 and telomerase reverse transcriptase (TERT) were overexpressed in fibroblasts from BWS patients and TGF-β-defective mice.
Hypomethylation within gene promoter regions and type 1 diabetes in discordant monozygotic twins.
Noble et al., Berkeley, United States. In J Autoimmun, Feb 2016
Initial results showed modest methylation differences between discordant MZ twins for the MHC region and T1D-associated CpG sites, BACH2, INS-IGF2, and CLEC16A (DNAm difference range: 2.2%-5.0%).
Epigenetic imprinting during assisted reproductive technologies: The effect of temporal and cumulative fluctuations in methionine cycling on the DNA methylation state.
Verschure et al., Amsterdam, Netherlands. In Mol Reprod Dev, Jan 2016
MEST, KCNQ1OT1, and IGF2- possess an altered DNA methylation profile in animal models, ART-conceived healthy children, and AS and BWS patients.
MECHANISMS IN ENDOCRINOLOGY: Novel genetic causes of short stature.
Kant et al., Leiden, Netherlands. In Eur J Endocrinol, Dec 2015
Besides well-defined causes of GH insensitivity (GHR, STAT5B, IGFALS, IGF1 defects), disorders of NFκB signalling, STAT3 and IGF2 have recently been discovered.
Non-Canonical (RANKL-Independent) Pathways of Osteoclast Differentiation and Their Role in Musculoskeletal Diseases.
Athanasou et al., Oxford, United Kingdom. In Clin Rev Allergy Immunol, Dec 2015
These humoral factors can generally be divided into those which, like RANKL, are tumour necrosis family (TNF) superfamily members and those which are not; the former include TNFα lymphotoxin exhibiting inducible expression and competing with herpes simplex virus glycoprotein D for herpesvirus entry mediator, a receptor expressed by T lymphocytes (LIGHT), a proliferation inducing ligand (APRIL) and B cell activating factor (BAFF); the latter include transforming growth factor beta (TGF-β), interleukin-6 (IL-6), IL-8, IL-11, nerve growth factor (NGF), insulin-like growth factor-I (IGF-I) and IGF-II.
Opposing intrinsic temporal gradients guide neural stem cell production of varied neuronal fates.
Lee et al., United States. In Science, Nov 2015
We found that two RNA-binding proteins, IGF-II mRNA-binding protein (Imp) and Syncrip (Syp), display opposing high-to-low and low-to-high temporal gradients with lineage-specific temporal dynamics.
Soluble M6P/IGFIIR in the circulation.
Kiess et al., Sydney, Australia. In Best Pract Res Clin Endocrinol Metab, Oct 2015
Soluble M6P/IGFIIR has the potential to be a significant carrier of IGF-II and mannose 6-P proteins in the circulation and play an important role as an antagonist to the cellular receptor.
Paternally Inherited IGF2 Mutation and Growth Restriction.
Eggermann et al., Tübingen, Germany. In N Engl J Med, Aug 2015
In humans, mutations in IGF1 or IGF1R cause intrauterine and postnatal growth restriction; however, data on mutations in IGF2, encoding insulin-like growth factor (IGF) II, are lacking.
Dynamics of DNA methylation at IGF2 in preterm and term infants during the first year of life: an observational study.
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.
A targetable GATA2-IGF2 axis confers aggressiveness in lethal prostate cancer.
Domingo-Domenech et al., New York City, United States. In Cancer Cell, Mar 2015
Mechanistically, direct upregulation of the growth hormone IGF2 emerged as a mediator of the aggressive properties regulated by GATA2.
Mutations in the SIX1/2 pathway and the DROSHA/DGCR8 miRNA microprocessor complex underlie high-risk blastemal type Wilms tumors.
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.
Progression to adrenocortical tumorigenesis in mice and humans through insulin-like growth factor 2 and β-catenin.
Hammer et al., Ann Arbor, United States. In Am J Pathol, 2012
With the combination of stabilized beta-catenin and elevated Igf2 expression, adrenal glands were larger, displayed earlier onset of hyperplasia, and developed more frequent macroscopic adenomas.
Genetic variants in IGF-I, IGF-II, IGFBP-3, and adiponectin genes and colon cancer risk in African Americans and Whites.
Millikan et al., Chapel Hill, United States. In Cancer Causes Control, 2012
Data indicate an inverse association between the insulin-like growth factor-2 (IGF-II) Apa1 A-variant and colon cancer risk (OR = 0.49, 95 % CI 0.28-0.88) in Whites only.
Akt1 and insulin-like growth factor 2 (Igf2) regulate placentation and fetal/postnatal development.
Soares et al., Kansas City, United States. In Int J Dev Biol, 2011
Data show that both Akt1-/- and Igf2-/- mice exhibited decreased placental weight, fetal weight and viability.
Prenatal famine and genetic variation are independently and additively associated with DNA methylation at regulatory loci within IGF2/H19.
Lumey et al., Leiden, Netherlands. In Plos One, 2011
Prenatal famine and genetic variation showed similar associations with IGF2/H19 methylation and their contributions were additive
Methylation defect in imprinted genes detected in patients with an Albright's hereditary osteodystrophy like phenotype and platelet Gs hypofunction.
Freson et al., Leuven, Belgium. In Plos One, 2011
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.
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