Ectophoma multirostrata strain:7a
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ABSTRACT:
PROVIDER: PRJNA500008 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Phoma multirostrata 7a Standard Draft genome sequencing
| PRJNA500110 | ENA
Project description:Flavobacterium sp. 7A strain:7A | isolate:CCM 8976 Genome sequencing
| PRJNA834341 | ENA
Project description:Sinorhizobium meliloti 7A Resequencing
| PRJNA501420 | ENA
Project description:Plesiomonas shigelloides strain:7A Genome sequencing
| PRJNA781848 | ENA
Project description:It is proposed that the impaired sympathoadrenal response to hypoglycemia induced by recurrent insulin-induced hypoglycemia (RH) is an adaptive phenomenon induced by specific changes in microRNA expression in the ventromedial hypothalamus (VMH). To test this hypothesis, genome-wide microRNAomic profiling of the VMH by RNA-sequencing was performed in control and RH treated rats. Differential expression analysis identified microRNA-7a-5p and microRNA-665 as potential mediators of this phenomenon. To further test this hypothesis, experiments were conducted consisting of targeted lentiviral-mediated overexpression of microRNA-7a-5p and downregulation of microRNA-665 in the VMH. Hyperinsulinemic hypoglycemic clamp experiments demonstrated that targeted overexpression of microRNA-7a-5p (but not downregulation of microRNA-665) in the VMH of RH rats restored the epinephrine response to hypoglycemia. This restored response to hypoglycemia was associated with a restoration of GABAA receptor gene expression. Finally, a direct interaction of microRNA-7a-5p with 3’-UTR of GABAA receptor α1-subunit (Gabra1) gene was demonstrated in a luciferase assay. These findings indicate that 1) the impaired sympathoadrenal response induced by RH is associated with changes in VMH microRNA expression, and 2) microRNA-7a-5p, possibly via direct downregulation of GABA receptor gene expression, may serve as a mediator of the altered sympathoadrenal response to hypoglycemia.
2019-10-17 | GSE138472 | GEO
Project description:Surface expression of C-X-C chemokine receptor type 4 (CXCR4) in acute myeloid leukemia (AML) has been reported to be an independent prognostic factor for disease relapse and survival. We previously reported that targeting the stromal-derived factor 1α (SDF-1α)/CXCR4 axis could overcome resistance of AML cells to chemotherapy both in vitro and in vivo. To further explore the mechanism of targeting CXCR4, in the current study we focused on the regulation of microRNA. Microarray analysis revealed that the hsa-let-7a microRNA was down-regulated in OCI-AML3 cells by SDF-1α treatment and increased after CXCR4 inhibition. To further investigate the role of hsa-let-7a in leukemia biology, we overexpressed it in AML cell lines, which resulted in decreased Bcl-xL protein expression and consequently enhanced cell sensitivity to the chemotherapeutic agent cytarabine, both in vitro and in vivo. We also identified the transcription factor Yin Yang 1 (YY1) as a mediator that links the SDF-1α/CXCR4 axis with hsa-let-7a. Western blotting and immunocytochemistry demonstrated a correlation between YY1 and CXCR4 activation. ChIP assay confirmed the binding of YY1 to pri-let-7a DNA fragments. In primary AML samples (n=50), high CXCR4 surface expression was associated with low hsa-let-7a levels (r2=0.53). Improved effects of cytarabine treatment associated with greatly extended survival of human AML carrying mice was observed in primary human AML overexpressing hsa-let-7a. On the basis of these results, we propose that CXCR4 regulation of hsa-let-7a microRNA through YY1 and transcriptional silencing of the Bcl-xL protein together identifies a novel mechanism by which CXCR4 functions to induce chemoresistance in AML cells.
2013-12-01 | GSE44828 | GEO
Project description:Bacillus cereus KPR-7A genome sequencing
| PRJNA303221 | ENA
Project description:Let-7 microRNAs (miRNAs) are a family of highly conserved well-established promoters of terminal differentiation that are expressed in all healthy adult tissues and frequently repressed in cancer cells. The tumour suppressive role of let-7 in a variety of cancers in vitro and in vivo has been widely documented and prompted these miRNAs to be candidate genes for miRNA replacement therapy. Reprogrammed metabolism, recently identified as a new hallmark of cancer, contributes to cancer cell growth, proliferation, invasiveness and drug resistance. In this study we identified a new metabolic role of let-7a in triple-negative breast cancer and metastatic melanoma cell lines. We show that let-7a down-regulates key anabolic enzymes, promotes oxidative phosphorylation and mitochondrial ROS formation accompanied by the up-regulation of the oxidative stress responsive genes. To assess if we could exploit these increased ROS levels for therapeutic purposes, we combined let-7a transfection with the antitumor drug doxorubicin. In both cancer types we observed a stronger response to the doxorubicin treatment in let-7a transfected cells. Pre-treatment with an antioxidant N-acetyl cysteine totally abolished this difference, indicating that the increased doxorubicin sensitivity of let-7a cells depends on the redox pathway. We demonstrated that let-7a plays a prominent role in regulating energy metabolism in cancer cells. We propose that a benefit from let-7 miRNA replacement therapy could come not only from the repression of oncogenic pathways targeted directly by let-7, but also by increased sensitivity to chemotherapeutic agents through indirect metabolic changes caused by let-7. Investigation of let-7a metabolic role in breast cancer and melanoma cells.
2015-12-31 | E-GEOD-60326 | biostudies-arrayexpress
Project description:Surface expression of C-X-C chemokine receptor type 4 (CXCR4) in acute myeloid leukemia (AML) has been reported to be an independent prognostic factor for disease relapse and survival. We previously reported that targeting the stromal-derived factor 1M-NM-1 (SDF-1M-NM-1)/CXCR4 axis could overcome resistance of AML cells to chemotherapy both in vitro and in vivo. To further explore the mechanism of targeting CXCR4, in the current study we focused on the regulation of microRNA. Microarray analysis revealed that the hsa-let-7a microRNA was down-regulated in OCI-AML3 cells by SDF-1M-NM-1 treatment and increased after CXCR4 inhibition. To further investigate the role of hsa-let-7a in leukemia biology, we overexpressed it in AML cell lines, which resulted in decreased Bcl-xL protein expression and consequently enhanced cell sensitivity to the chemotherapeutic agent cytarabine, both in vitro and in vivo. We also identified the transcription factor Yin Yang 1 (YY1) as a mediator that links the SDF-1M-NM-1/CXCR4 axis with hsa-let-7a. Western blotting and immunocytochemistry demonstrated a correlation between YY1 and CXCR4 activation. ChIP assay confirmed the binding of YY1 to pri-let-7a DNA fragments. In primary AML samples (n=50), high CXCR4 surface expression was associated with low hsa-let-7a levels (r2=0.53). Improved effects of cytarabine treatment associated with greatly extended survival of human AML carrying mice was observed in primary human AML overexpressing hsa-let-7a. On the basis of these results, we propose that CXCR4 regulation of hsa-let-7a microRNA through YY1 and transcriptional silencing of the Bcl-xL protein together identifies a novel mechanism by which CXCR4 functions to induce chemoresistance in AML cells. MicroRNA expression profiling of OCI-AML3 cell lines treated with CXCR4 antagonist or SDF-1M-NM-1. OCI-AML3 cells were treated with 100 ng/mL SDF-1M-NM-1 or 250 nM POL6326 (a CXCR4 antagonist, Allschwil, Switzerland), total RNA was extracted at specific time points (1, 2, 4, and 8 h), and miRNA expression profiling was performed
2013-12-01 | E-GEOD-44828 | biostudies-arrayexpress