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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, Insulin-Like Growth Factor I, CAN, HAD, IGF-I receptor
Papers using Insulin-Like Growth Factor II antibodies
LYVE-1, the lymphatic system and tumor lymphangiogenesis
Supplier
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
Insulin-Like Growth Factor II (IGF-II) Inhibits IL-1β-Induced Cartilage Matrix Loss and Promotes Cartilage Integrity in Experimental Osteoarthritis.
New
Zeng et al., Boston, United States. In J Cell Biochem, 26 Jun 2015
In this study, we found that the expression of Insulin-like Growth Factor II (IGF-II) was reduced in articular cartilage in human OA patients as well as in the murine experimental OA model of destabilization of the medial meniscus (DMM).
Rapid molecular evolution across amniotes of the IIS/TOR network.
New
Schwartz et al., Taipei, Taiwan. In Proc Natl Acad Sci U S A, 19 Jun 2015
In reptiles, positively selected sites cluster on the binding surfaces of insulin-like growth factor 1 (IGF1), IGF1 receptor (IGF1R), and insulin receptor (INSR); whereas in mammals, positively selected sites clustered on the IGF2 binding surface, suggesting that these hormone-receptor binding affinities are targets of positive selection.
Integrated genomic analyses identify frequent gene fusion events and VHL inactivation in gastrointestinal stromal tumors.
New
Sohn et al., Seoul, South Korea. In Oncotarget, 30 Apr 2015
Transcriptome sequencing revealed 328 gene fusions, and the most frequently involved fusion events were associated with IGF2 fused to several partner genes including CCND1, FUS, and LASP1.
Insulin and IGF receptor signalling in neural-stem-cell homeostasis.
Review
New
Wood et al., Newark, United States. In Nat Rev Endocrinol, Mar 2015
IGF-II is of particular interest as a result of its production by the choroid plexus and presence in cerebrospinal fluid (CSF).
Mutations in the SIX1/2 pathway and the DROSHA/DGCR8 miRNA microprocessor complex underlie high-risk blastemal type Wilms tumors.
New
Impact
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.
Taxane resistance in prostate cancer mediated by AR-independent GATA2 regulation of IGF2.
New
Impact
Balk et al., Seattle, United States. In Cancer Cell, Mar 2015
In this issue of Cancer Cell, Vidal and colleagues identify increased GATA2 and its AR-independent transactivation of IGF2 as a mechanism that can mediate taxane resistance through activation of IGF1/insulin receptor signaling.
A targetable GATA2-IGF2 axis confers aggressiveness in lethal prostate cancer.
New
Impact
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.
PU.1 Is Identified as a Novel Metastasis Suppressor in Hepatocellular Carcinoma Regulating the miR-615-5p/IGF2 Axis.
New
Wang et al., Zhengzhou, China. In Asian Pac J Cancer Prev, Dec 2014
Overexpression of PU.1 caused a dramatic increase of pri-, pre- and mature miR-615-5p, as well as a marked decrease of miR-615-5p target gene IGF2.
Therapeutic targeting of liver inflammation and fibrosis by nanomedicine.
Review
New
Tacke et al., Aachen, Germany. In Hepatobiliary Surg Nutr, Dec 2014
HSC, the main collagen-producing cells during fibrosis, are currently targeted using nanoconstructs that recognize the mannose 6-phosphate and insulin-like growth factor II, peroxisome proliferator activated receptor 1, platelet-derived growth factor (PDGF) receptor β, or integrins.
Insulin/Insulin-like growth factors in cancer: new roles for the aryl hydrocarbon receptor, tumor resistance mechanisms, and new blocking strategies.
Review
New
Tomblin et al., Huntington, United States. In Front Endocrinol (lausanne), Dec 2014
Molecular targeting therapies that have been used in solid tumors include anti-IGF1R antibodies, anti-IGF1/IGF2 antibodies, and small molecule inhibitors that suppress IGF1R and IR kinase activity.
[Changes in markers of proliferation, neoangiogenesis and plasminogen activation system in rectal cancer tissue].
New
Cheryarina et al., In Eksp Klin Gastroenterol, Dec 2014
I. Concurrent expressionof IGF-I, IGF-II, TGF-β1 and VEGF-Aanditsreceptorinmalignanttumortissue, as well as increasedplasmin release from proenzyme and MMP-3 activationis apparently associatedwith the formation ofpathogenic mechanism of vasculature development in moderately differentiated adenocarcinoma of the rectum.
Portrait of the PI3K/AKT pathway in colorectal cancer.
Review
New
Lothe et al., Oslo, Norway. In Biochim Biophys Acta, Dec 2014
In colorectal cancer the most commonly observed pathway changes are IGF2 overexpression, PIK3CA mutations and PTEN mutations and deletions.
Oncogenic transformation of diverse gastrointestinal tissues in primary organoid culture.
New
Impact
Kuo et al., Stanford, United States. In Nat Med, Jul 2014
Colon organoid culture functionally validated the microRNA miR-483 as a dominant driver oncogene at the IGF2 (insulin-like growth factor-2) 11p15.5 CRC amplicon, inducing dysplasia in vitro and tumorigenicity in vivo.
IGF binding proteins in cancer: mechanistic and clinical insights.
Review
New
Impact
Baxter, Sydney, Australia. In Nat Rev Cancer, May 2014
IGFBPs also function in the pericellular and intracellular compartments to regulate cell growth and survival - they interact with many proteins, in addition to their canonical ligands IGF-I and IGF-II.
IGF-IR Targeted Therapy: Past, Present and Future.
Review
Varewijck et al., Rotterdam, Netherlands. In Front Endocrinol (lausanne), 2013
Activation of the IR-A by insulin-like growth factor-II (IGF-II) bypasses the IGF-IR and its inhibition.
Progression to adrenocortical tumorigenesis in mice and humans through insulin-like growth factor 2 and β-catenin.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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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