Figure 3
Figure 3. Mapping of coding sequences of mouse ADAMTS13 cDNA and the domain structures of the predicted proteins. (A) A full-length coding sequence consisting of 29 exons was cloned from a FVB/NJ mouse, whereas 2 coding sequences (IAP-a and IAP-b) were cloned from a C57BL/6J mouse. Both IAP variants ended with an exon consisting of sequences from the LTR of IAP and its 5′ flanking intronic sequence. IAP-b differed from IAP-a in that its exon 15 contained extra residues from intron 15 and lacked the exon 16 of IAP-a. As estimated by real-time RT-PCR using 2 primer pairs indicated in this panel, IAP-b accounted for 26% of the total ADAMTS13 mRNA. (B) The predicted domain structures of the 3 forms of ADAMTS13 cloned from mouse livers. Both IAP variants ended with a 16-residue sequence derived from the aberrant exon 24. A 61-residue sequence in the spacer domain of IAP-a was replaced by a novel sequence of 52 residues encoded by the extraneous sequence of exon 15.

Mapping of coding sequences of mouse ADAMTS13 cDNA and the domain structures of the predicted proteins. (A) A full-length coding sequence consisting of 29 exons was cloned from a FVB/NJ mouse, whereas 2 coding sequences (IAP-a and IAP-b) were cloned from a C57BL/6J mouse. Both IAP variants ended with an exon consisting of sequences from the LTR of IAP and its 5′ flanking intronic sequence. IAP-b differed from IAP-a in that its exon 15 contained extra residues from intron 15 and lacked the exon 16 of IAP-a. As estimated by real-time RT-PCR using 2 primer pairs indicated in this panel, IAP-b accounted for 26% of the total ADAMTS13 mRNA. (B) The predicted domain structures of the 3 forms of ADAMTS13 cloned from mouse livers. Both IAP variants ended with a 16-residue sequence derived from the aberrant exon 24. A 61-residue sequence in the spacer domain of IAP-a was replaced by a novel sequence of 52 residues encoded by the extraneous sequence of exon 15.

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