Abstract
This update of the I blood group system (Cooling L. Polylactosamines, there's more than meets the "Ii": a review of the I system. Immunohematology 2010;26:133-55) continues to show the Ii antigens to be increasingly recognized as important posttranslational modifiers regulating cell adhesion, signaling, differentiation, and cancer. Ii antigens can modulate the immune response through the galectin lattice, as well as influence specific protein-protein interactions. Changes in GCNT2 and I expression accompany stem cell differentiation and are associated with tumor progression in melanoma and breast and colon cancer. Regulation of GCNT2 expression varies between cell types and differentiation. In red blood cell differentiation, GCNT2 is regulated by methylation, microRNAs, and mitogen-activated protein kinase signaling pathways. Methylation and microRNAs also play a prominent role in altering GCNT2 expression in several epithelial cancers. In congenital cataracts, GCNT2 mutations may account for 4-6 percent of all cases. GCNT2 may be particularly susceptible to gene deletion and rearrangements due to the density of Alu-repeat elements.
Highlights
An update on the I blood group systemThis update of the I blood group system
In red blood cell differentiation, GCNT2 is regulated by methylation, microRNAs, and mitogen-activated protein kinase signaling pathways
Using the erythroleukemia line K562, Twu and colleagues were able to map upstream regulation of GCNT2C by ERK2 and SHP2.15 Treatment of K562 cells with sodium butyrate to induce erythroid differentiation resulted in increased GCNT2C mRNA and I antigen expression, with equivalent decreases in phosphorylated ERK2 and c/EBPα-p21
Summary
This update of the I blood group system Changes in GCNT2 and I expression accompany stem cell differentiation and are associated with tumor progression in melanoma and breast and colon cancer. Regulation of GCNT2 expression varies between cell types and differentiation. In red blood cell differentiation, GCNT2 is regulated by methylation, microRNAs, and mitogen-activated protein kinase signaling pathways. Methylation and microRNAs play a prominent role in altering GCNT2 expression in several epithelial cancers. GCNT2 mutations may account for 4–6 percent of all cases. GCNT2 may be susceptible to gene deletion and rearrangements due to the density of Alu-repeat elements.
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