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MiR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP]

ABSTRACT: miR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP]

PROVIDER: PRJNA631767 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11772816.fastq.gz	Fastqsanger.gz
	SRR11772817.fastq.gz	Fastqsanger.gz
	SRR11772818.fastq.gz	Fastqsanger.gz
	SRR11772819.fastq.gz	Fastqsanger.gz
	SRR11772820.fastq.gz	Fastqsanger.gz

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miR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP]

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miR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP

Project description:miR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP

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miR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP

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Mir-146a wild-type 3ʹ sequence identity is dispensable for proper innate immune function in vivo

Project description:A long-prevailing model has held that the “seed” region (nucleotides 2-8) of a microRNA is typically sufficient to mediate target recognition and repression. However, numerous recent studies, both within the context of defining miRNA/target pairs by direct physical association and by directly assessing this model in vivo in C. elegans have brought this model into question. To test the importance of miRNA 3' pairing in vivo, in a mammalian system, we engineered a mutant murine mir-146a allele in which the 5' half of the mature microRNA retains the sequence of the wild-type mir-146a but the 3ʹ half has been altered to be anti-complementary to the wild-type miR-146a sequence. Mice homozygous or hemizygous for this mutant allele are phenotypically indistinguishable from wild-type controls and do not recapitulate any of the immunopathology previously described for mir-146a-null mice. Our results strongly support the conclusion that 3ʹ pairing is dispensable in the context of the function of a key mammalian microRNA.

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miR-146a Pulldown-sequencing data

Project description:miR-146a Pulldown-sequencing data

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miR-146a target identification in gastric cancer

Project description:We have found expression of miR-146a up-regulated in gastric cancer. To identify new targets of miR-146a we profiled the transcriptome after miR-146a over-expression in the human gastric cancer cell line SNU638. SNU638 cells were transfected in triplicates with 50 nM miR-146a or control (siGlo) using Lipofectamine 2000. Total RNA was harvested 24 h after transfection using Trizol reagent. There are a total of six arrays included in this experiment, including three biological replicates of mRNA expression after miR-146a over-expression and three controls in SNU638 cells.

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Transcription profiling by array of human Jurkat T cells either over-expressing miR-146a or with miR-146a knockdown

Project description:Screening the differetial expressed genes with Jurkat-146a(miR-146a over expression),Jurkat-sponge(miR-146a knockdown),Jurkat-FF3(vector control)

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Identification of miR-146a target genes in mouse monocyte subsets

Project description:To gain insight into the mechanisms underlying miR-146a-mediated modulation of Ly6Chigh monocyte function, we compared the expression profiles of Ly6Chigh and Ly6Clow monocytes in miR-146a+/+ (WT) versus miR-146a-/- (KO) conditions.

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