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Analysis of delayed changes in expression of miRNA in rat kidneys: role of miR-34a

ABSTRACT: Analysis of delayed changes in expression of miRNA in rat kidneys: role of miR-34a

PROVIDER: PRJNA472182 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7187420_1.fastq.gz	Fastqsanger.gz
	SRR7187420_2.fastq.gz	Fastqsanger.gz
	SRR7187460_1.fastq.gz	Fastqsanger.gz
	SRR7187460_2.fastq.gz	Fastqsanger.gz
	SRR7187432_1.fastq.gz	Fastqsanger.gz

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Analysis of delayed changes in expression of miRNA in rat kidneys: role of miR-34a

Project description:We used a rat model of whole body (except one hind limb that was shielded) x-ray irradiation to profile the microRNA (miRNA) in kidneys at 35 days after radiation. Small RNA from normal and irradiated (with or without lisinopril) Wistar rat kidneys were analyzed by next-generation sequencing and the changes by radiation and lisinopril were identified by deRNA-seq. MiR-34a-5p was increased after irradiation.

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2019-10-14 | PXD015278 | Pride

Comparing two approaches of miR-34a target identification, biotinylated-miRNA pulldown vs miRNA overexpression

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Project description:Analysis NCI-H1299 lung cancer cells transfected with synthetic oligo mimics for microRNAs (miRNAs) miR-34a and ghR-34a. We developed a 30-nucleotide single-strand RNA (ssRNA), termed “guide hairpin RNA (ghR),” that has a physiological function similar to that of miRNA and siRNA. The ghR caused no innate cytokine response either in vitro or in vivo. In addition, its structure does not contain a passenger strand seed sequence, reducing the potential for off-target effects relative to existing short RNA reagents. Systemic injection of ghR-form miR-34a (ghR-34a) suppressed tumor growth in a mouse model of RAS-induced lung cancer. Furthermore, ghR-34a functioned in a Dicer- and Ago2-independent manner. This novel RNAi technology may provide a novel, safe, and effective nucleic acid drug platform that will increase the clinical usefulness of nucleic acid therapy. MiR-34a–targeted mRNAs regulated by mRNA degradation rather than translational inhibition were identified using microarray data from miR-34 and ghR-34a transfectants.

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