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Results identified SRSF9 protein as one of the factors involved in modulating the splicing of the DDC mutated (c.714+4A>T) transcript.
The splicing factor SRSF9 is a key factor that serves to restrict the editing of numerous protein-coding and non-coding sites to the brain. The results highlight the importance of SRSF9 as an editing regulator and suggest potential roles for other splicing factors.
Dehydroepiandrosterone (DHEA) and cortisol modulate SRSF9 and SRSF3 in a different way and data suggest that the anti-glucocorticoid effect of DHEA, among other mechanisms, is also exerted by modulating the expression of proteins involved in the splicing of the GR pre-mRNA.
Report no correlation between expression of glucocorticoid receptor isoforms and SRp30c.
Overexpression of SRSF9 and SRSF1 promote beta-catenin accumulation via the recruitment of beta-catenin mRNA and by enhancing its translation in an mTOR-dependent manner.
Relative levels of SRp20, SRp30c, and SRp40 in TM cells control differential expression of the two alternatively spliced isoforms of the GR and thereby regulate GC responsiveness.
these data indicated that tumor suppressive miR-1 induces apoptosis through direct inhibition of SRSF9 in bladder cancer.
These results suggest that SRp30c can activate human papillomavirus type 16 L1 mRNA expression via a bimodal mechanism: directly by stimulating splicing to late splice sites and indirectly by inhibiting competing early splice sites.
SRp30c can function as a repressor of 3' splice site utilization and suggest that the SRp30c-CE9 interaction may contribute to the control of hnRNP A1 alternative splicing.
SRp30c protein is an interacting protein of YB-1
Serine-arginine-rich protein p30 directs alternative splicing of glucocorticoid receptor pre-mRNA to glucocorticoid receptor beta in neutrophils.
Results suggest that bombesin-induced expression of SRp30c affects gllucorticoid receptor (GR) pre-mRNA splicing, leading to increased GR beta expression and contributing to glucocorticoid resistance in PC cells.
Study shows that PTB can function as an anti-repressor molecule to counteract the splicing inhibitory activity of SRp30c.
SRp30c stimulates splicing to the downstream 5' splice site of Bcl-x(L), thereby attenuating the repressive effect of upstream U1 snRNP binding sit
findings indicate the importance of arginine methylation for the subnuclear localization of SFRS9.
Data show that editing of Cav1.3 calcium channel (CaV1.3) was potently inhibited by serine/arginine-rich splicing factor 9 (SRSF9).
cooperative action of multiple SR proteins in the regulation of GnRH pre-mRNA splicing; SRp30c specifically binds to both ESE3 and ESE4
The protein encoded by this gene is a member of the serine/arginine (SR)-rich family of pre-mRNA splicing factors, which constitute part of the spliceosome. Each of these factors contains an RNA recognition motif (RRM) for binding RNA and an RS domain for binding other proteins. The RS domain is rich in serine and arginine residues and facilitates interaction between different SR splicing factors. In addition to being critical for mRNA splicing, the SR proteins have also been shown to be involved in mRNA export from the nucleus and in translation. Two pseudogenes, one on chromosome 15 and the other on chromosome 21, have been found for this gene.
SR splicing factor 9
, pre-mRNA-splicing factor SRp30C
, splicing factor, arginine/serine-rich 9
, splicing factor, arginine/serine rich 9
, serine/arginine-rich splicing factor 9