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. 2010 Apr 12;38(15):5130–5140. doi: 10.1093/nar/gkq198

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Published by Oxford University Press (2010).

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — The AflIII–NheI region of FLT1 intron 13 is required to significantly reduce splicing of exon 13 to exon 14. (A) Schematic representation of human FLT1 gene in the region of exons 13 and 14. The position of the putative proximal poly(A) signal sequence, the known distal poly(A) signal sequences and the restriction sites used to map cis-elements is shown. (B) RPA demonstrating relative abundance of intronic sFlt1 and spliced Flt1 in COS-7 cells transfected with a series of Flt1 minigene constructs. The full-length construct leads primarily to intronic sFlt1, and deletions that do not remove the distal polyA sites do not substantially increase the abundance of spliced Flt1. Deletion of the region between AflIII and NheI, has a significant effect on processing to spliced Flt1. (C) Pooled quantitated data from several experiments with the Flt1 to sFlt1 ratio in each condition expressed as fold increase compared to the ratio in the full-length construct. n = 4, mean ± SEM, P < 0.001, ANOVA, *P < 0.05 compared to each of the other samples.