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Noncanonical Formation of SNX5 Gene-Derived Circular RNA Regulates Cancer Growth

ABSTRACT: To investgate the funcitonal role of STAU1 on the formation of circSNX5. We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells (replicate)

ORGANISM(S): Homo sapiens

PROVIDER: GSE214084 | GEO | 2024/06/19

REPOSITORIES: GEO

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Noncanonical Formation of SNX5 Gene-Derived Circular RNA Regulates Cancer Growth

Project description:To investgate the funcitonal role of STAU1 on the formation of circSNX5. We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells (replicate)

2024-06-19 | GSE213634 | GEO

Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception

Project description:To investgate the funcitonal role of Unc80 by RNA editing mechanism

2024-06-10 | GSE269152 | GEO

STAU1 selectively regulates the expression of inflammatory and immune response genes and alternative splicing of nerve growth factor receptor signaling genes

Project description:To study the potential targets and functions of STAU1 which might be related to neuropathic pain, we obtained STAU1-regulated transcriptome in HeLa cells. High-throughput RNA sequencing(RNA-seq) were performed for HeLa cells and control cells to define the comprehensive gene expression profiles and identify the genome-wide alternative splicing events regulated by STAU1.

2020-10-20 | GSE136890 | GEO

Staufen1 regulates a variety of mammalian transcripts

2007-12-26 | GSE6679 | GEO

siRNA of human HeLa cells reveals Staufen1 regulates a variety of mammalian transcripts

Project description:It is currently unknown how extensively the double-stranded RNA binding protein Staufen (Stau)1 is utilized by mammalian cells to regulate gene expression. To date, Stau1 binding to the 3â untranslated region (3âUTR) of ARF1 mRNA has been shown to target ARF1 mRNA for Stau1-mediated mRNA decay (SMD). ARF1 SMD depends on translation and recruitment of the nonsense-mediated mRNA decay factor Upf1 to the ARF1 3âUTR by Stau1. Here, we use microarray analyses to examine changes in the abundance of cellular mRNAs that occur when Stau1 is depleted. Results indicate that 1.1% and 1.0% of the 11,569 HeLa-cell transcripts that were analyzed are, respectively, upregulated and downregulated at least two-fold in three independently performed experiments. Additionally, we localize the Stau1 binding site to the 3âUTR of four mRNAs that we define as natural SMD targets. Together, these and substantiating results suggest that Stau1 influences the expression of a wide variety of physiologic transcripts and metabolic pathways. Experiment Overall Design: We report the results of three independently performed microarray analyses that examined changes in the abundance of transcripts from HeLa-cell genes upon Stau1 depletion. HeLa cells were transiently transfected with either a nonspecific Control small interfering (si)RNA or Stau1 siRNA. Stau1 siRNA reduced the level of cellular Stau1 to as little as 4% of normal, where normal is defined as the level in the presence of Control siRNA (data not shown). RNA from three independently performed transfections was separately hybridized to microarrays.

2008-06-15 | E-GEOD-6679 | biostudies-arrayexpress

Noncanonical frizzled signaling regulates cell polarity of growth plate chondrocytes.

Project description:Bone growth is driven by cell proliferation and the subsequent hypertrophy of chondrocytes arranged in columns of discoid cells that resemble stacks of coins. However, the molecular mechanisms that direct column formation and the importance of columnar organization to bone morphogenesis are not known. Here, we show in chick that discoid proliferative chondrocytes orient the division plane to generate daughter cells that are initially displaced laterally and then intercalate into the column. Downregulation of frizzled (Fzd) signaling alters the dimensions of long bones and produces cell-autonomous changes in proliferative chondrocyte organization characterized by arbitrary division planes and altered cell stacking. These defects are phenocopied by disruption of noncanonical effector pathways but not by inhibitors of canonical Fzd signaling. These findings demonstrate that the regulation of cell polarity and cell arrangement by noncanonical Fzd signaling plays important roles in generating the unique morphological characteristics that shape individual cartilage elements.

| S-EPMC2685929 | biostudies-literature

Transcriptome analysis revealed that SMD regulates neuronal differentiation.

Project description:Transcriptome analysis from Staufen-mediated mRNA (SMD) targets during differentiation confirmed that STAU1 was a key factor in neuronal differentiation.

2017-02-27 | GSE94948 | GEO

Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue [expression profiling]

Project description:To investgate the role of EBF1 in human adipocyte, we performed global expression profiling in human adipocytes transfected with siRNA targeting EBF1.

2014-05-22 | GSE42680 | GEO

Noncanonical K27-linked polyubiquitination of TIEG1 regulates Foxp3 expression and tumor growth.

Project description:Earlier, we demonstrated the essential role of Kruppel-like transcription factor, TIEG1, in TGF-?-induced regulatory T cell (Treg) development. In this article, we demonstrate that IL-6, which promotes Th17 development, abrogated TIEG1 nuclear translocation and inhibited TGF-?-induced Treg development. Tyrosine kinase Tyk2-mediated phosphorylation of TIEG1 at Tyr179 promoted noncanonical K-27-linked polyubiquitination, which inhibited TIEG1 nuclear translocation. To test the role of TIEG1-regulated Treg/Th17 development in antitumor immunity, we analyzed TRAMP-C2 tumor growth in TIEG1(-/-) mice. The defective Treg development and elevated Th17 response resulted in enhanced immune reactivity in the tumor and inhibition of TRAMP-C2 tumor growth in TIEG1(-/-) mice. Thus, our results uncovered a novel regulatory mechanism that modulates Tregs and may regulate tumor progression.

| S-EPMC3914214 | biostudies-literature

3'READS+RIP defines differential Staufen1 binding to alternative 3'UTR isoforms and reveals structures and sequence motifs influencing binding and polysome association

Project description:Using 3ʹ region extraction and deep sequencing coupled to ribonucleoprotein immunoprecipitation (3’READS+RIP), together with reanalyzing previous STAU1 binding and RNA structure data, we delineate STAU1 interactions transcriptome-wide, including binding differences between alternative polyadenylation (APA) isoforms. Consistent with previous reports, RNA structures are dominant features for STAU1 binding to CDSs and 3ʹUTRs. Overall, relative to short 3ʹUTR counterparts, longer 3ʹUTR isoforms of genes have stronger STAU1 binding, most likely due to a higher frequency of RNA structures, including specialized IRAlus. However, a sizable fraction of genes express transcripts showing the opposite trend, attributable to AU-rich sequences in their alternative 3'UTRs, possibly recruiting antagonistic RBPs and/or destabilizing STAU1-binding RNA structures. Using STAU1-knockout cells, we show that strong STAU1 binding to mRNA 3'UTRs generally enhances polysome association. However, IRAlus have little impact on STAU1-mediated polysome association despite having strong interactions with the protein.

2020-11-05 | GSE148771 | GEO

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