Fig. 3From: A disease-causing variant of COL4A5 in a Chinese family with Alport syndrome: a case seriesMutation analysis of the intronic variant. A Analysis using Alamut Visual v.2.11 has shown that the variant c.911-14A > C generated the novel potential splicing acceptor site (red rectangle). B Exon 17 to 19 spanning the intronic variant was cloned into vector H492. C Splicing products in cell lines were confirmed by Sanger sequencingBack to article page