Project description:HnRNPLL was identified as a critical regulator of CD45 alternative splicing in a lentiviral shRNA screen. RNAi-mediated depletion of hnRNPLL eliminated the activation-induced induced transition from the CD45RA to the CD45RO isoform. HnRNPLL is induced during the process of T cell activation, raising the possibility that it regulates a broad program of alternative splicing in activated T cells. To test this possibility and to identify additional potential targets of hnRNPLL, we performed exon array analysis on RNA isolated from five cellular conditions: 1) activated peripheral CD4+ T cells, 2) peripheral CD4+ T cells infected with a control shRNA directed against GFP, 3) peripheral CD4+ T infected with an shRNA directed against hnRNPLL, 4) naïve cord blood CD4+ T cells, and 5) cord blood CD4+ T cells that had been activated with anti-CD3 and anti-CD28 for 24 hours. The RNA was hybridized to Affymetrix human exon arrays and the hybridization signals were analyzed with XRAYTM software (Biotique). Using stringent filters for non-expressed probesets, we identified 132 genes that showed significant alternative exon usage (p<0.01) in response to hnRNPLL knockdown, but not in response to shGFP infection. Of these 132 genes, 36 also showed significant alternative exon usage in response to activation of cord blood cells, which results in an approximate 5-fold increase in hnRNPLL expression. We thus conclude that induction of hnRNPLL represents a mechanism by which cells can rapidly shift their transcriptomes during the process of T cell activation. This SuperSeries is composed of the SubSeries listed below.

2008-06-20 | GSE11834 | GEO

HnRNPLL is a global regulator of alternative splicing in activated T cells

Project description:HnRNPLL was identified as a critical regulator of CD45 alternative splicing in a lentiviral shRNA screen. RNAi-mediated depletion of hnRNPLL eliminated the activation-induced induced transition from the CD45RA to the CD45RO isoform. HnRNPLL is induced during the process of T cell activation, raising the possibility that it regulates a broad program of alternative splicing in activated T cells. To test this possibility and to identify additional potential targets of hnRNPLL, we performed exon array analysis on RNA isolated from five cellular conditions: 1) activated peripheral CD4+ T cells, 2) peripheral CD4+ T cells infected with a control shRNA directed against GFP, 3) peripheral CD4+ T infected with an shRNA directed against hnRNPLL, 4) naÃ¯ve cord blood CD4+ T cells, and 5) cord blood CD4+ T cells that had been activated with anti-CD3 and anti-CD28 for 24 hours. The RNA was hybridized to Affymetrix human exon arrays and the hybridization signals were analyzed with XRAYTM software (Biotique). Using stringent filters for non-expressed probesets, we identified 132 genes that showed significant alternative exon usage (p<0.01) in response to hnRNPLL knockdown, but not in response to shGFP infection. Of these 132 genes, 36 also showed significant alternative exon usage in response to activation of cord blood cells, which results in an approximate 5-fold increase in hnRNPLL expression. We thus conclude that induction of hnRNPLL represents a mechanism by which cells can rapidly shift their transcriptomes during the process of T cell activation. This SuperSeries is composed of the following subset Series: GSE11832: naive/activated ANOVA group GSE11833: LL-sh4/uninfected/shGFP ANOVA group

2010-09-15 | E-GEOD-11834 | biostudies-arrayexpress

Alternative CD44 splicing identifies epithelial prostate cancer cells from the mesenchymal counterparts.

Project description: Not available

| S-EPMC4391735 | biostudies-literature

WNT5A inhibits metastasis and alters splicing of Cd44 in breast cancer cells.

Project description: Not available

| S-EPMC3590134 | biostudies-literature

The RNA-binding protein hnRNPLL induces a T cell alternative splicing program delineated by differential intron retention in polyadenylated RNA.

Project description: Not available

| S-EPMC4053824 | biostudies-literature

Identification of common genetic variation that modulates alternative splicing.

Project description: Not available