Complete Deficiency of Glycophorin A in Red Blood Cells From Mice With Targeted Inactivation of the Band 3 (AE1) Gene

摘要: Glycophorin A is the major transmembrane sialoglycoprotein of red blood cells. It has been shown to contribute expression MN and Wright group antigens, act as a receptor for malaria parasite Plasmodium falciparum Sendai virus, along with anion transporter, band 3, may mechanical properties cell membrane. Several lines evidence suggest close interaction between glycophorin 3 during their biosynthesis. Recently, we have generated mice where was completely eliminated by selective inactivation AE1 exchanger gene, thus allowing us study effect on membrane proteins. In this report, show that -/- cells contain protein 4.1, adducin, dematin, p55, C. contrast, are devoid (GPA), assessed Western blot immunocytochemistry techniques, whereas polymerase chain reaction (PCR) confirmed presence GPA mRNA. Pulse-label pulse-chase experiments not incorporated in rapidly degraded cytoplasm. Based these findings other published evidence, propose plays chaperone-like role, which necessary recruitment plasma