Fig. 3.
Fig. 3. Analysis of IIb cDNA and the IIb gene in patient MS. (A) Amplification of IIb cDNA from patient MS by RT-PCR. Two hundred fifty nanograms of total cellular RNA from MS or a normal control was amplified by RT-PCR using primers IIb3 and IIb4. The PCR products were electrophoresed on 1.5% agarose gel. (B) Nucleotide sequence analysis of IIb cDNA from patient MS. The cDNA PCR fragments were subcloned into pUC19, and nucleotides were sequenced. (C) Nucleotide sequence analysis of the IIb gene from patient MS. Nucleotide of the IIb gene from patient MS or a normal control was amplified by PCR using primers IIbE16 and IIbI18 and sequenced. (D) Schematic diagram indicates the mechanism of exon18 skipping of the platelet IIb mRNA.

Analysis of IIb cDNA and the IIb gene in patient MS. (A) Amplification of IIb cDNA from patient MS by RT-PCR. Two hundred fifty nanograms of total cellular RNA from MS or a normal control was amplified by RT-PCR using primers IIb3 and IIb4. The PCR products were electrophoresed on 1.5% agarose gel. (B) Nucleotide sequence analysis of IIb cDNA from patient MS. The cDNA PCR fragments were subcloned into pUC19, and nucleotides were sequenced. (C) Nucleotide sequence analysis of the IIb gene from patient MS. Nucleotide of the IIb gene from patient MS or a normal control was amplified by PCR using primers IIbE16 and IIbI18 and sequenced. (D) Schematic diagram indicates the mechanism of exon18 skipping of the platelet IIb mRNA.

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