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Knockdown of ILF2/ILF3 (NF45/NF90) in the gastric cancer cell line SGC7901

ABSTRACT: Knockdown of ILF2/ILF3 (NF45/NF90) in the gastric cancer cell line SGC7901

PROVIDER: PRJNA678681 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13067192_1.fastq.gz	Fastqsanger.gz
	SRR13067192_2.fastq.gz	Fastqsanger.gz
	SRR13067193_1.fastq.gz	Fastqsanger.gz
	SRR13067193_2.fastq.gz	Fastqsanger.gz
	SRR13067194_1.fastq.gz	Fastqsanger.gz

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Knockdown of ILF2/ILF3 (NF45/NF90) in the gastric cancer cell line SGC7901

Project description:Our data showed that lncRNA ELF3-AS1 could bind on the exon1 of ELF3-201 to form a double-stranded RNA molecule. This double-stranded RNA could interact with ILF2/ILF3 complex. To explore the biofunction of the interaction between ELF3-AS1 and ILF2/ILF3 complex, loss-of-function studies regarding ILF2 and ILF3 were performed in SGC7901 cell line. RNA sequencing studies showed that knockdown of ILF3 significantly decreased ELF3-AS1, while knockdown of ILF2 significantly increased ELF3-AS1 and NF90 expression. Our data revealed that ILF2/ILF3 complex interacted with ELF3-AS1/ELF3 double-stranded RNA and regulated their transcripts stability.

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NF45 and NF90/NF110 coordinately regulate ESC pluripotency and differentiation

Project description:While years of investigation have elucidated many aspects of embryonic stem cell (ESC) regulation, the contributions of post-transcriptional and translational mechanisms to the pluripotency network remain largely unexplored. In particular, little is known in ESCs about the function of RNA binding proteins (RBPs), the protein agents of post-transcriptional regulation. We performed an unbiased RNAi screen of RBPs in an ESC differentiation assay and identified two related genes, NF45 (Ilf2) and NF90/NF110 (Ilf3), whose knockdown promoted differentiation to an epiblast-like state. Characterization of NF45 KO, NF90+NF110 KO, and NF110 KO ESCs showed that loss of NF45 or NF90+NF110 impaired ESC proliferation and led to dysregulated differentiation down embryonic lineages. Additionally, we found that NF45 and NF90/NF110 physically interact and influence the expression of each other at different levels of regulation. Globally across the transcriptome, NF45 KO ESCs and NF90+NF110 KO ESCs show similar expression changes. Moreover, NF90+NF110 RNA immunoprecipitation (RIP)-seq in ESCs suggested that NF90/NF110 directly regulate proliferation, differentiation, and RNA-processing genes. Our data support a model in which NF45, NF90, and NF110 operate in feedback loops that enable them, through both overlapping and independent targets, to help balance the push and pull of pluripotency and differentiation cues.

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Project description:We used ChIP-seq to characterize the genome-wide binding sites of NF90/ILF3 in K562 erythroleukemia cells.

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Project description:The complex of NF90 and NF45 is known to participate in transcriptional regulation, mRNA stabilization and microRNA biogenesis in vitro. However, the physiological function of the NF90-NF45 complex is still unclear. To elucidate its functions, we generated NF90-NF45 double transgenic (dbTg) mice. Robust expression of NF90 and NF45 was detected in skeletal muscle. As mentioned above, NF90-NF45 complex is involved in regulation of genes via transcription and RNA metabolism. To identify genes regulated by NF90-NF45, we performed comprehensive analyses of mRNA expression in quadriceps of wild-type (WT) and NF90-NF45 dbTg mice. mRNA expression profile in quadriceps comparing WT and NF90-NF45 dbTg mice.

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Genome-wide binding sites of NF90/ILF3 in K562 erythroleukemia cells

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