Fig. 4.
Fig. 4. ASRA. (A) The region around exon 23 of the IIb gene was amplified by PCR using primers IIbE23 and IIbE24Pvu II, followed by digestion with PvuII. The A → C substitution creates a restriction site forPvu II and yields 202-bp and 20-bp fragments. The resulting fragments were electrophoresed in a 6% polyacrylamide gel. (B) The region around exon 18 of the IIb gene was amplified by PCR using primers IIbE17A and IIbI18, followed by digestion withAvr II. Avr II digestion of the PCR products yields 330-bp and 218-bp fragments in the normal allele. The G → A substitution abolished a restriction site for Avr II. The resulting fragments were electrophoresed in a 1.5% agarose gel. F, M, P, and C denote DNA from the patient’s father, mother, patient (MS), and control, respectively. Undigested PCR fragment from the control is also shown (U). Marker: ◊X174 digested with Hae III.

ASRA. (A) The region around exon 23 of the IIb gene was amplified by PCR using primers IIbE23 and IIbE24Pvu II, followed by digestion with PvuII. The A → C substitution creates a restriction site forPvu II and yields 202-bp and 20-bp fragments. The resulting fragments were electrophoresed in a 6% polyacrylamide gel. (B) The region around exon 18 of the IIb gene was amplified by PCR using primers IIbE17A and IIbI18, followed by digestion withAvr II. Avr II digestion of the PCR products yields 330-bp and 218-bp fragments in the normal allele. The G → A substitution abolished a restriction site for Avr II. The resulting fragments were electrophoresed in a 1.5% agarose gel. F, M, P, and C denote DNA from the patient’s father, mother, patient (MS), and control, respectively. Undigested PCR fragment from the control is also shown (U). Marker: ◊X174 digested with Hae III.

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