{"database":"ENA","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Fastqsanger.gz":["ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/068/SRR12210268/SRR12210268_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/064/SRR12210264/SRR12210264_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/066/SRR12210266/SRR12210266_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/065/SRR12210265/SRR12210265_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/065/SRR12210265/SRR12210265_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/063/SRR12210263/SRR12210263_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/068/SRR12210268/SRR12210268_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/067/SRR12210267/SRR12210267_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/064/SRR12210264/SRR12210264_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/063/SRR12210263/SRR12210263_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/066/SRR12210266/SRR12210266_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/067/SRR12210267/SRR12210267_2.fastq.gz"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["University of Liverpool"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA645887"],"long_description":["Pulmonary arterial hypertension (PAH) is a complex pulmonary vascular disease characterised by excessive vascular endothelial and smooth muscle cell proliferation, inflammation, and fibrosis, resulting in increased pulmonary vascular resistance and right ventricular hypertrophy. Circulating levels of endothelial miR-150 are reduced in PAH and act as an independent predictor of patient survival. Mechanistic links between endothelial miR-150 levels and vascular dysfunction in PAH are not well understood.8.0) was used for polyadenylated RNA selection using poly-T oligo attached magnetic beads, followed by the fragmentation of poly-A containing mRNA. Cleaved RNA fragments were copied into first strand cDNA using reverse transcriptase with random primers. The cDNA was further converted into double-stranded DNA that was end-repaired to incorporate the specific index adapters for multiplexing, followed by purification and amplification. The amplified libraries were examined using an Agilent 2100 Bioanalyzer and a Qubit. The samples for this study were pooled alongside 12 additional samples from other studies and together the 18 samples were sequenced across 4 lanes (2 x 100 bp) on a HiSeq 2500 using TruSeq SBS V3-HS kit (Illumina Inc.) in high output run mode (average of 34.4 million reads per sample)."],"tag":["xref:EuropePMC:PMC7733016"],"repository":["ENA"],"description_synonyms":["9430057C20Rik, HH, l(3)hh, biological signaling, PLIP, pulmonary hypertension, Myosin regulatory light chain interacting protein, 6.3.2.-, bar, IDOL, Arterial Hypertension, CG4637, Hh, CG12249, AW228700, anon-WO0134654.19, DmelCG4637, bar3, DUSP23, 1, DmelCG12249, Mir, MIR, with hereditary hemorrhagic telangiectasia, Pulmonary, primary, Miranda, Diphosphatidylglycerol, PAH with overt features of venous/capillaries involvement, l(3)neo56, l(3)neo57, MONDOA, PPH1, Mrt, Mira, Diphosphatidylglycerols, Pph1 with Hht, Inducible degrader of the LDL-receptor, mir, PVOD/PCH, Pulmonary Arterial, MOSP, pulmonary arterial hypertension, signalling, Hypertension, Myosin regulatory light chain-interacting protein, signalling process, anon-WO0182946.19, bar-3, signaling process, MIRA, bHLHe36, PHT., Idol, Fenfluramine-associated, Cardiolipin, Dexfenfluramine-associated, single organism signaling, hg"],"additional_accession":[]},"is_claimable":false,"name":"","description":"Mir-150-PTPMT1-Cardiolipin signaling in Pulmonary Arterial Hypertension","dates":{"last_updated":"2023-05-17","first_public":"2020-07-25"},"accession":"PRJNA645887","cross_references":{}}