Words similar to igf-ii
Example sentences for: igf-ii
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In addition, choroid plexus expresses insulin, IGF-I, and IGF-II receptors [ 11 47 ] ., as well as large amounts of IGF-II that is secreted into the CSF [ 47 ] . CSF contains insulin/IGFs and 5-HT [ 48 ] in concentrations high enough to activate their respective receptors in choroid plexus, suggesting that this signaling mechanism may occur in vivo . It has been suggested that 5-5HT 2C receptors in choroid plexus may be tonically activated, due to CSF 5-HT concentrations near the EC 50 , thus tonically inhibiting CSF production.
Modulation of this mitogenic pathway occurs in part via the M6P/IGF2R, which functions in the internalization and degradation of IGF-II [ 10 ] . M6P/IGF2R is also important in activation of TGF-β, a potent growth inhibitor for most cell types, and in binding, transport and activation of lysosomal enzymes, such as cathepsins [ 12 13 ] . It has been shown that M6P/IGF2R expression is significantly reduced in both rat and human hepatocellular carcinomas [ 14 ] . Loss of hetorozygosity (LOH) at the M6P/IGF2 receptor gene locus on 6q26-27 coupled with somatic point mutations in the remaining allele has recently been demonstrated in liver and breast cancers [ 15 16 17 18 19 20 21 22 23 ] . In addition, somatic mutations of the M6P/IGF2R gene were also found in prostate cancer, lung carcinoma, and genetically unstable cancers of the endometrium, brain, stomach and colorectum [ 24 25 26 27 28 29 ] . The findings of LOH and mutations of M6P/IGF2R in a wide variety of tumor types have led to the proposition that the M6P/IGF2R is a tumor suppressor gene.
This is consistent with previous observations that M6P/IGF2R knockout mice displayed generalized increased growth and cardiomygaly (resulting from cardiac myocyte hyperplasia) [ 34 ] , and that antisense-mediated reduction of M6P/IGF2R expression enhances tumorigenicity in JEG-3 cells [ 43 ] . Thus, loss or mutation of M6P/IGF2R may contribute to development and progression of tumors via different pathways: by increasing the mitogenic activity of IGF-II and decreasing the apoptotic signaling of TGF-β and lysosomal proteases.
For treatment with IGF-II, cells were incubated with 50 ng/ml IGF-II after infection with Ad-GFP/IGF2R-Rz or Ad-GFP.
M6P/IGF2R-null mice display global hyperplasia that coincides with elevated levels of IGF-II.
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