ABSTRACT The gene FLT1 produces at least two transcripts from a common transcription start site: full-length Flt1 contains 30 exons encoding a membrane-bound VEGF receptor; soluble Flt1 (sFlt1) shares the ï¬rst 13 exons but utilizes poly(A) signal sequences within intron 13 to create a transcript that lacks downstream exons. To address the mechanisms that regulate human sFlt1, we mapped the 3 end of sFlt1 mRNA and deï¬ned the full extent of its 3 untranslated region (UTR). We identiï¬ed a 3.2 Kb sFlt1 transcript that is cleaved within an alternatively spliced exon downstream of exon 14 and is predicted to encode a C-terminal variant of sFlt1 with an unusual polyserine tail. sFlt1 mRNA cleavage sites within intron 13 were identiï¬ed in human placenta and in vascular endothelium by ribonuclease protection assay (RPA). A proximal and two distal mRNA cleavage sites were identiï¬ed by RPA downstream of consensus polyadenylation signals that create variant transcripts with a 3 UTR ranging from 30 bases to 4 Kb. Northern blot analysis and 3 rapid ampliï¬cation of cDNA ends (RACE) in placenta conï¬rmed the existence of distal intronic sFlt1 cleavage sites that give rise to a sFlt1 transcript of 7 Kb. The identity of
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Intronic polyadenylation signal sequences and alternate splicing generate human soluble Flt1 variants and regulate the abundance of soluble Flt1 in the placenta
Christie P. Thomas , Janet I. Andrews , and Kang Z. Liu
Follow The FASEB Journal
, Volume 21 (14): 3885
Fed of American Socs for Experimental Biology – Dec 1, 2007
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