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ATAC-seq for SK-HEP-1 cell line with or without sirolimus treatment

ABSTRACT: ATAC-seq for SK-HEP-1 cell line with or without sirolimus treatment

PROVIDER: PRJNA1001395 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25496856_1.fastq.gz	Fastqsanger.gz
	SRR25496856_2.fastq.gz	Fastqsanger.gz
	SRR25496857_1.fastq.gz	Fastqsanger.gz
	SRR25496857_2.fastq.gz	Fastqsanger.gz

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ATAC-seq for SK-HEP-1 cell line with or without sirolimus treatment

Project description:The openness of chromatin affects the expression and regulation of genes. In order to figure out the changes of transcriptional factors after sirolimus treatment in hepatocellular carcinoma, ATAC-seq was performed for human hepatocellular carcinoma cell line SK-HEP-1. Here, we found that a series of transcriptional factors, including E2F1, SP1, M2F1, etc. enhanced binding to DNA after sirolimus treatment.

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Genome-wide maps of H3K27me3 modification sites in sk-hep-1,sk-hep-1-shEZH2 and LO2 cells.

Project description:We report the application of chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) for high-throughput profiling of H3K27me3 modifications in sk-hep-1(sk), sk-hep-1-shEZH2 (sks) and LO2 cells. Following standard ChIP procedure, 10 ng of each DNA sample was used for Illumina sequencing. Statistically significant ChIP-enriched regions (peaks) were identified by sk vs sks (p-value threshold of 10-2) or sk vs LO2 (p-value threshold of 10-3). Enriched peaks were annotated by the nearest gene using the newest UCSC RefSeq database. We identify genes modified by EZH2-mediated H3K27me3. This study provides insights into these down stream genes modified by EZH2 regulated H3K27me3 in HCC cell lines.

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N6-methyladenosine (m6A) RIP-seq in SK-Hep-1 cells

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N6-methyladenosine (m6A) RIP-seq in SK-Hep-1 cells

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Sirolimus induced phosphaturia

Project description:Introduction: The kidney is the major arbiter of extracellular phosphate homeostasis. The vast majority of glomerular filtrated phosphate is reabsorbed in the proximal tubule. Posttransplant phosphaturia is common and aggravated by sirolimus immunosuppression. The cause of sirolimus induced phosphaturia however remains elusive. Results: The urine phosphate/creatinine ratio was higher and serum phosphate was lower in sirolimus treated rats, fractional excretion of phosphate was elevated and renal tubular phosphate reabsorption was reduced suggesting a renal cause for hypophosphatemia. PTH was lower in sirolimus treated rats. FGF 23 levels were unchanged at day 2 but lower in sirolimus treated rats after 7 days. Brush border membrane vesicle phosphate uptake was not altered in sirolimus treated groups or by direct incubation with sirolimus. mRNA, protein abundance, and subcellular transporter distribution of NaPi-IIa, Pit-2 and NHE3 were not different between groups but NaPi-IIc mRNA expression was lower at day 7. Transcriptome analyses revealed candidate genes that could be involved in the phosphaturic response. Discussion: Sirolimus caused a selective renal phosphate leakage which was not mediated by NaPi-IIa or NaPi-IIc regulation or localization. We hypothesize that another mechanism such as a basolateral phosphate transporter may be responsible for the sirolimus induced phosphaturia. Male Wistar rats received sirolimus or vehicle for 7 days (1.5mg/kg) and were placed in individual metabolic cages for eight days allowing a 24 hour adaption period to the metabolic cage environment. At the end of the experiments rats were anesthetized by inhalation of Isoflurane/air and blood samples and kidneys were collected.

2012-09-24 | GSE35048 | GEO

Sirolimus induced phosphaturia

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Effect of knockdown LINC01089 on gene expression in SK-Hep-1 cells

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