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RNA-Seq identifies alternative splicing of CRBN induced by ILF3 KO

ABSTRACT: RNA-Seq identifies alternative splicing of CRBN induced by ILF3 KO

PROVIDER: PRJNA645653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12202071_1.fastq.gz	Fastqsanger.gz
	SRR12202071_2.fastq.gz	Fastqsanger.gz
	SRR12202072_1.fastq.gz	Fastqsanger.gz
	SRR12202072_2.fastq.gz	Fastqsanger.gz
	SRR12202073_1.fastq.gz	Fastqsanger.gz

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RNA-Seq identifies alternative splicing of CRBN induced by ILF3 KO

Project description:We present a first-in-class GSPT1-selective CELMoD, CC-90009, which is currently in a phase 1 clinical trial for the treatment of relapsed or refractory (R/R) AML (CC-90009-AML-001; NCT02848001). Biochemical, structural and molecular characterization supports that CC-90009 coopts the CUL4-DDB1-CRBN-RBX1 (CRL4-CRBN) E3 ubiquitin ligase complex to selectively target GSPT1 for ubiquitination and proteasomal degradation, culminating in rapid induction of apoptosis and growth inhibition in AML cell lines and patient leukemic blasts. Knockout of ILF2/ILF3 decreased the production of full-length CRBN transcript via modulating CRBN mRNA alternative splicing, leading to significant downregulation of cereblon expression and hence diminished response to CC-90009.

2021-02-05 | GSE154257 | GEO

Expression and alternative splicing data from 1-month-old Rbfox1 KO brain

Project description:Rbfox1 regulates the alternative splicing of many transcripts in neurons. We have characterized the Rbfox1-dependent changes in expression and alternative splicing by comparing Rbfox1-KO brain to WT brain. In this dataset, we include the splicing and expression data obtained from dissected WT and Rbfox1 KO mouse brains. 6 total samples were analyzed: brains from 3 WT male mice and 3 Rbfox1 KO male mice, all 1 month of age.

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A network of DZF proteins controls alternative splicing regulation and fidelity [eCLIP-seq]

Project description:Proteins containing DZF (domain associated with zinc fingers) modules play important roles throughout gene expression, from transcription to translation. Derived from nucleotidyltransferases but lacking catalytic residues, DZF domains serve as heterodimerization surfaces between DZF protein pairs. Three DZF proteins are widely expressed in mammalian tissues, ILF2, ILF3, and ZFR, which form mutually exclusive ILF2-ILF3 and ILF2-ZFR heterodimers. Using eCLIP-Seq, we find that ZFR binds across broad intronic regions to regulate the alternative splicing of cassette and mutually exclusive exons. ZFR preferentially binds dsRNA in vitro and is enriched on introns containing conserved dsRNA elements in cells. Many splicing events are similarly altered upon depletion of any of the three DZF proteins; however, we also identify independent and opposing roles for ZFR and ILF3 in alternative splicing regulation. Along with widespread involvement in cassette exon splicing, the DZF proteins control the fidelity and regulation of over a dozen highly validated mutually exclusive splicing events. Our findings indicate that the DZF protein complexes form a complex regulatory network that leverages dsRNA binding by ILF3 and ZFR to modulate splicing regulation and fidelity.

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Proteomics analysis of macrophage with ILF3 dificiency (ILF3-KO) and expressing (Control).

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Transcriptome analysis of alternative splicing events regulated by SRSF10 reveals position-dependent splicing modulation.

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