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- W2364888601 abstract "Fibroblast growth factor(FGF) can promote cell proliferation and induce angiogenesis.It has been correlated with tumorigenesis.A mutant form of the FGF receptor 2IIIc(FGFR2),P253R,which is found in Apert syndrome,has a higher affinity for FGF2 and causes excessive autocrine and paracrine signaling,leading to skeletal dysplasia.Total RNA was extracted from human placental tissue and the ectodomain of FGFR2Ⅲc(wsFGFR2) was amplified using reverse-transcriptase polymerase chain reaction(RT-PCR).The P253R mutant(msFGFR2,P253R mutant found in Apert syndrome which has a higher affinity for FGF ligands) was obtained through overlap-extension PCR by using wsFGFR2 as template.msFGFR2 was cloned into a pET3c vector and expressed them in the form of inclusion bodies in Escherichia coli strain BL21(DE3).Successfully refolded proteins were isolated by gel chromatography and purified by heparin affinity chromatography.The refolding yield of msFGFR2 was 12%,with purity higher than 95%.MTT cell proliferation assay showed that msFGFR2 significantly inhibited the stimulatory effect of FGF2 on NIH3T3 cell proliferation.msFGFR2 also effectively inhibited the proliferation of the prostate cancer cell line DU145,indicating that msFGFR2 could block the FGF signaling pathway and had a potential clinical application in cancer therapy." @default.
- W2364888601 created "2016-06-24" @default.
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- W2364888601 date "2011-01-01" @default.
- W2364888601 modified "2023-09-24" @default.
- W2364888601 title "Expression,Refolding,and Activity Studies of the FGFR2IIIc Soluble Ectodomain Mutant P253R" @default.
- W2364888601 hasPublicationYear "2011" @default.
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