Ontology highlight
ABSTRACT:
PROVIDER: PRJNA909943 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22572825_1.fastq.gz | Fastqsanger.gz | |||
| SRR22572825_2.fastq.gz | Fastqsanger.gz | |||
| SRR22572826_1.fastq.gz | Fastqsanger.gz | |||
| SRR22572826_2.fastq.gz | Fastqsanger.gz | |||
| SRR22572827_1.fastq.gz | Fastqsanger.gz |
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Project description:We used Solexa sequencing technology to probe the gene expression of dorsal skin tissues from three full-sib Rex rabbits of different colors. The number of expressed genes in each sample was approximately 14,700. Compared with the chinchilla Rex rabbit control sample, the numbers of genes that exhibited greater than a 2-fold change in expression with a false discovery rate of ≤0.001 in the black rabbit sample and white rabbit sample were 1,809 and 460, respectively, and the number of common differentially expressed genes was 257.Of the 257 genes, 32 genes that were upregulated in sample B and downregulated in sample W. The FABP7 gene was the only gene that was downregulated in the B sample and upregulated in the W sample
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Project description:Sequencing of rex rabbit with different phenotype
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Project description:1) Background: TP53 gene mutations occur in 70% of oesophageal adenocarcinomas (OACs). Given the central role of p53 in controlling cellular response to therapy we investigated the role of mutant (mut-) p53 and SLC7A11 in a CRISPR-mediated JH-EsoAd1 TP53 knockout model. (2) Methods: Response to 2 Gy irradiation, cisplatin, 5-FU, 4-hydroxytamoxifen and endoxifen was assessed, followed by a TaqMan OpenArray qPCR screening for differences in miRNA expression. (3) Results: Knockout of mut-p53 resulted in increased chemo- and radioresistance (2 Gy survival fraction: 38% vs. 56%, p<0.0001) and in altered miRNA expression levels. Target mRNA pathways analyses indicated several potential mechanisms of treatment resistance. SLC7A11 knockdown restored radiosensitivity (2 Gy SF: 46% vs. 73%; p=0.0239), possibly via enhanced sensitivity to oxidative stress. Pathway analysis of the predicted mRNA targets of differentially expressed miRNAs indicated potential involvement in several pathways associated with apoptosis, ribosomes as well as in p53 signalling pathways. (4) Discussion: These results provide a better understanding of the important role of SLC7A11 in cancer metabolism and redox balance and the influence of p53 on these processes. Inhibition of the SLC7A11-gluthatione axis may represent a promising approach to overcome resistance associated with mut-p53.
2021-05-31 | GSE171965 | GEO
Project description:The objective of this comparison was to identify the impact of rex deletion on the transcriptome of Streptococcus pneumoniae D39. This comparison showed that the transcriptional regulator, Rex acts as a transcriptional repressor of a number of genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in niacin uptake and biosynthesis in the presence of NADH. In this study, we investigated the transcriptomic response of Streptococcus pneumoniae D39 to NADH. Transcriptome comparison of the D39 wild-type grown in chemically-defined medium (CDM) with 0 mg/ml NADH to 0.5 mg/ml NADH revealed elevated expression of various genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in the transport and biosynthesis of niacin. Microarray results were further confirmed by β-galactosidase assays. Promoter-lacZ fusions assays and microarray studies showed that the transcriptional regulator, Rex acts as a transcriptional repressor of a number of genes/operons (adhB1, fba, hemH, rex, gapN, nirC, pncB, gap, adhE, and adhB2) involved in niacin uptake and biosynthesis in the presence of NADH. The putative operator site of Rex in the promoter regions of Rex-regulated genes is predicted and confirmed by promoter mutational experiments.
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Project description:Understanding the genomic and epigenetic mechanisms of drug resistance in pediatric acute lymphoblastic leukemia (ALL) is critical for further improving treatment. The role of transcriptomic response in conferring resistance to l-asparaginase (LASP) is poorly understood, beyond asparagine synthetase (ASNS). We defined reproducible LASP response genes in LASP resistant and sensitive ALL cells lines as well as primary leukemia samples from newly diagnosed patients. Defining ATF4 target genes in ALL cell lines using ChIP-seq revealed 25% of genes that changed expression after LASP treatment were direct targets of the ATF4 transcription factor. SLC7A11 was found to be a response gene in cell lines and patient samples as well as a direct target of ATF4. SLC7A11 was also one of only 2.4% of response genes with basal level gene expression that also correlated with LASP ex vivo resistance in primary leukemia cells. Experiments using chemical inhibition of SLC7A11 with sulfasalazine, gene overexpression, and partial gene knockout recapitulated LASP resistance or sensitivity in ALL cell lines. These findings show the importance of assessing changes in gene expression following treatment with antileukemic agent for their association with drug resistance and highlight that many response genes may not differ in their basal expression in drug resistant leukemia cells.
2022-04-15 | GSE200830 | GEO
Project description:Understanding the genomic and epigenetic mechanisms of drug resistance in pediatric acute lymphoblastic leukemia (ALL) is critical for further improving treatment. The role of transcriptomic response in conferring resistance to l-asparaginase (LASP) is poorly understood, beyond asparagine synthetase (ASNS). We defined reproducible LASP response genes in LASP resistant and sensitive ALL cells lines as well as primary leukemia samples from newly diagnosed patients. Defining ATF4 target genes in ALL cell lines using ChIP-seq revealed 25% of genes that changed expression after LASP treatment were direct targets of the ATF4 transcription factor. SLC7A11 was found to be a response gene in cell lines and patient samples as well as a direct target of ATF4. SLC7A11 was also one of only 2.4% of response genes with basal level gene expression that also correlated with LASP ex vivo resistance in primary leukemia cells. Experiments using chemical inhibition of SLC7A11 with sulfasalazine, gene overexpression, and partial gene knockout recapitulated LASP resistance or sensitivity in ALL cell lines. These findings show the importance of assessing changes in gene expression following treatment with antileukemic agent for their association with drug resistance and highlight that many response genes may not differ in their basal expression in drug resistant leukemia cells.
2022-04-15 | GSE174499 | GEO
Project description:Compared to the well-established roles of apoptosis in tumor suppression, the roles and regulatory mechanisms of ferroptosis, a non-apoptotic form of cell death, in tumor biology remain much less understood. BRCA1-associated protein 1 (BAP1) encodes a nuclear de-ubiquitinating (DUB) enzyme to reduce histone 2A ubiquitination (H2Aub) on chromatin, and is a tumor suppressor in several human cancers. Here, integrated transcriptomic, epigenomic, and cancer genomic analyses link BAP1 to metabolism-related biological processes, including oxidative stress response, and identify cystine transporter SLC7A11 as a BAP1-repressed target gene with high relevance to BAP1-mediated tumor suppression in human cancers. Functional studies reveal that BAP1, in a DUB-dependent manner, decreases H2Aub occupancy on the SLC7A11 promoter and represses SLC7A11 expression, and that BAP1 inhibits cystine uptake and promotes ferroptosis through repressing SLC7A11 expression. Finally, we show that BAP1 inhibits tumor development partly through SLC7A11, and that cancer-associated BAP1 mutants lose their abilities to repress SLC7A11 and to promote ferroptosis. Together, the results of our study show that BAP1 executes its tumor suppression function at least partly through its regulation of SLC7A11 and ferroptosis, and uncover a previously unappreciated mechanism coupling ferroptosis to tumor suppression.
2018-07-05 | GSE101987 | GEO