Matches in SemOpenAlex for { <https://semopenalex.org/work/W2170702502> ?p ?o ?g. }
- W2170702502 endingPage "1258" @default.
- W2170702502 startingPage "1247" @default.
- W2170702502 abstract "To identify human intronic sequences associated with 5' splice site recognition, we performed a systematic search for motifs enriched in introns downstream of both constitutive and alternative cassette exons. Significant enrichment was observed for U-rich motifs within 100 nucleotides downstream of 5' splice sites of both classes of exons, with the highest enrichment between positions +6 and +30. Exons adjacent to U-rich intronic motifs contain lower frequencies of exonic splicing enhancers and higher frequencies of exonic splicing silencers, compared with exons not followed by U-rich intronic motifs. These findings motivated us to explore the possibility of a widespread role for U-rich motifs in promoting exon inclusion. Since cytotoxic granule-associated RNA binding protein (TIA1) and TIA1-like 1 (TIAL1; also known as TIAR) were previously shown in vitro to bind to U-rich motifs downstream of 5' splice sites, and to facilitate 5' splice site recognition in vitro and in vivo, we investigated whether these factors function more generally in the regulation of splicing of exons followed by U-rich intronic motifs. Simultaneous knockdown of TIA1 and TIAL1 resulted in increased skipping of 36/41 (88%) of alternatively spliced exons associated with U-rich motifs, but did not affect 32/33 (97%) alternatively spliced exons that are not associated with U-rich motifs. The increase in exon skipping correlated with the proximity of the first U-rich motif and the overall U-richness of the adjacent intronic region. The majority of the alternative splicing events regulated by TIA1/TIAL1 are conserved in mouse, and the corresponding genes are associated with diverse cellular functions. Based on our results, we estimate that approximately 15% of alternative cassette exons are regulated by TIA1/TIAL1 via U-rich intronic elements." @default.
- W2170702502 created "2016-06-24" @default.
- W2170702502 creator A5002958608 @default.
- W2170702502 creator A5003361977 @default.
- W2170702502 creator A5008426210 @default.
- W2170702502 creator A5011210102 @default.
- W2170702502 creator A5032292978 @default.
- W2170702502 creator A5040287362 @default.
- W2170702502 creator A5052837962 @default.
- W2170702502 creator A5056025103 @default.
- W2170702502 creator A5081824595 @default.
- W2170702502 creator A5085182984 @default.
- W2170702502 date "2008-05-02" @default.
- W2170702502 modified "2023-10-02" @default.
- W2170702502 title "A systematic analysis of intronic sequences downstream of 5′ splice sites reveals a widespread role for U-rich motifs and TIA1/TIAL1 proteins in alternative splicing regulation" @default.
- W2170702502 cites W1504845338 @default.
- W2170702502 cites W1549994062 @default.
- W2170702502 cites W1964072966 @default.
- W2170702502 cites W1969697265 @default.
- W2170702502 cites W1971158461 @default.
- W2170702502 cites W1971278266 @default.
- W2170702502 cites W1975406504 @default.
- W2170702502 cites W1975687045 @default.
- W2170702502 cites W1978386292 @default.
- W2170702502 cites W1985991078 @default.
- W2170702502 cites W1986113553 @default.
- W2170702502 cites W1988692621 @default.
- W2170702502 cites W1994823144 @default.
- W2170702502 cites W1994940904 @default.
- W2170702502 cites W2001952613 @default.
- W2170702502 cites W2003605043 @default.
- W2170702502 cites W2015249201 @default.
- W2170702502 cites W2015809578 @default.
- W2170702502 cites W2019518393 @default.
- W2170702502 cites W2023648355 @default.
- W2170702502 cites W2024267851 @default.
- W2170702502 cites W2026671856 @default.
- W2170702502 cites W2028279880 @default.
- W2170702502 cites W2030409202 @default.
- W2170702502 cites W2031172990 @default.
- W2170702502 cites W2034337754 @default.
- W2170702502 cites W2034691490 @default.
- W2170702502 cites W2037139598 @default.
- W2170702502 cites W2039599894 @default.
- W2170702502 cites W2043435109 @default.
- W2170702502 cites W2045300068 @default.
- W2170702502 cites W2054696719 @default.
- W2170702502 cites W2063318299 @default.
- W2170702502 cites W2064207737 @default.
- W2170702502 cites W2080290909 @default.
- W2170702502 cites W2080379289 @default.
- W2170702502 cites W2083827172 @default.
- W2170702502 cites W2087815448 @default.
- W2170702502 cites W2096413283 @default.
- W2170702502 cites W2102337459 @default.
- W2170702502 cites W2102992354 @default.
- W2170702502 cites W2106154073 @default.
- W2170702502 cites W2108141237 @default.
- W2170702502 cites W2108876548 @default.
- W2170702502 cites W2114858580 @default.
- W2170702502 cites W2115149771 @default.
- W2170702502 cites W2115282694 @default.
- W2170702502 cites W2116185451 @default.
- W2170702502 cites W2117660195 @default.
- W2170702502 cites W2118823143 @default.
- W2170702502 cites W2118994793 @default.
- W2170702502 cites W2121006508 @default.
- W2170702502 cites W2125391335 @default.
- W2170702502 cites W2125887220 @default.
- W2170702502 cites W2132295996 @default.
- W2170702502 cites W2132451711 @default.
- W2170702502 cites W2133059678 @default.
- W2170702502 cites W2146950091 @default.
- W2170702502 cites W2147016321 @default.
- W2170702502 cites W2155345824 @default.
- W2170702502 cites W2158020008 @default.
- W2170702502 cites W2158048358 @default.
- W2170702502 cites W2158463967 @default.
- W2170702502 cites W2159864549 @default.
- W2170702502 cites W2166797651 @default.
- W2170702502 cites W2169361401 @default.
- W2170702502 cites W2170074416 @default.
- W2170702502 cites W2337463877 @default.
- W2170702502 cites W46722564 @default.
- W2170702502 doi "https://doi.org/10.1101/gr.073155.107" @default.
- W2170702502 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2493427" @default.
- W2170702502 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18456862" @default.
- W2170702502 hasPublicationYear "2008" @default.
- W2170702502 type Work @default.
- W2170702502 sameAs 2170702502 @default.
- W2170702502 citedByCount "90" @default.
- W2170702502 countsByYear W21707025022012 @default.
- W2170702502 countsByYear W21707025022013 @default.
- W2170702502 countsByYear W21707025022014 @default.
- W2170702502 countsByYear W21707025022015 @default.
- W2170702502 countsByYear W21707025022016 @default.
- W2170702502 countsByYear W21707025022017 @default.
- W2170702502 countsByYear W21707025022018 @default.