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Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165772 | GEO | 2022/01/28

REPOSITORIES: GEO

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Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [RNA-Seq]

Project description:About 70% of human genes carry multiple polyadenylation signals, and mRNA 3’end formation is dynamically regulated under different physiological conditions. Global 3’end shortening through alternative polyadenylation (APA) correlates with enhanced cellular proliferation, and 3’ untranslated region (UTR) shortening is a widespread phenomenon in tumour cells, where it appears to enhance tumorigenic properties. However, the mechanisms responsible for this dynamic APA regulation remain incompletely understood. Here we show that transcription factor Sp1 binds directly to RNA in vivo and is a common repressor of distal poly (A) site usage. RNA-sequencing (RNA-seq) analysis identified 2344 genes (36% of total mapped mRNA transcripts) with lengthened 3’UTRs upon Sp1 depletion. Sp1 preferentially binds in vivo within the 3’UTRs of many of these lengthened transcripts and inhibits cleavage at distal sites by interacting physically with subunits of the core cleavage and polyadenylation (CPA) machinery. The 3’UTR lengths of Sp1 target genes in breast cancer patient RNA-seq data correlate with Sp1 expression levels, implicating Sp1-mediated APA regulation in modulating tumorigenic properties. Taken together, our findings reveal an important mechanism for dynamic APA regulation by unraveling a novel function of Sp1.

2022-01-28 | GSE165771 | GEO

Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [CLIP-seq]

2022-01-28 | GSE165739 | GEO

Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [ChIP-Seq]

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Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1

Project description:Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1

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Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [CLIP-seq]

Project description:Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [CLIP-seq]

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Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [ChIP-Seq]

Project description:Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [ChIP-Seq]

| PRJNA695451 | ENA

Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [RNA-Seq]

Project description:Regulation of alternative polyadenylation by the C2H2-zinc finger protein Sp1 [RNA-Seq]

| PRJNA697861 | ENA

Multiparameter functional diversity of human C2H2 zinc finger proteins

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-10-25 | E-GEOD-76496 | biostudies-arrayexpress

Multiparameter functional diversity of human C2H2 zinc finger proteins

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-10-25 | GSE76496 | GEO

Myocardial ischemic preconditioning upregulated protein 1(Mipu1):zinc finger protein 667 - a multifunctional KRAB/C2H2 zinc finger protein.

Project description:Myocardial ischemic preconditioning upregulated protein 1 (Mipu1) is a newly discovered upregulated gene produced in rats during the myocardial ischemic preconditioning process. Mipu1 cDNA contains a 1824-base pair open reading frame and encodes a 608 amino acid protein with an N-terminal Krüppel-associated box (KRAB) domain and classical zinc finger C2H2 motifs in the C-terminus. Mipu1 protein is located in the cell nucleus. Recent studies found that Mipu1 has a protective effect on the ischemia-reperfusion injury of heart, brain, and other organs. As a nuclear factor, Mipu1 may perform its protective function through directly transcribing and repressing the expression of proapoptotic genes to repress cell apoptosis. In addition, Mipu1 also plays an important role in regulating the gene expression of downstream inflammatory mediators by inhibiting the activation of activator protein-1 and serum response element.

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