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Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells [miRNA-Seq]

ABSTRACT: Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells [miRNA-Seq]

PROVIDER: PRJNA847203 | ENA |

REPOSITORIES: ENA

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Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells [miRNA-Seq]

Project description:To investigate the effect of gene alteration of Miat and Mtdh in mouse stem-like MB cells. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. Miat and Mtdh cooperate to promote medulloblastoma tumorigenesis and treatment resistance by regulating the biogenesis of a subset of microRNAs that target genes involved in these processes.

2022-07-29 | GSE205694 | GEO

Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells

Project description:Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells

| PRJNA847198 | ENA

Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells [RNA-Seq]

Project description:Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells [RNA-Seq]

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Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells [RNA-Seq]

Project description:To investigate the effect of gene alteration of Miat in mouse stem-like MB cells. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. Miat and Mtdh cooperate to promote medulloblastoma tumorigenesis and treatment resistance by regulating the biogenesis of a subset of microRNAs that target genes involved in these processes.

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lncRNA/mRNA expression profiling of miR-200c-overexpressing MDA-MB-231 cells

Project description:MiR-200c is a well-studied miRNA that is involved in stemness, the epithelial-mesenchymal transition, chemoresistance, radioresistance, and invasion/metastasis of various cancer cells. To obtain an overview of the lncRNA/mRNA regulated by miR-200c signaling in breast-cancer cell lines, we performed global lncRNA/mRNA-expression profiling on MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c cells.

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Transcriptome profiling of left ventricles from systemic MIAT knockout mice

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Chromatin accessibility analysis of MIAT sufficient and MIAT deficient Th17 cells by ATAC-seq

Project description:T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. We found that MIAT deficiency leads to chromatin accessibility at several loci including IL17A promoter.

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lncRNA and mRNA expression of cytokine treated MDA-MB-231 cells

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Gene expression of depletion of lncRNA Miat in mouse stem-like MB cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-29 | GSE205695 | GEO

Long Intergenic Noncoding RNA MIAT Contributes to Human Th17 Cell Differentiation

Project description:T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. RNA-seq analysis identified genes implicated in Th17 differentiation and functions as MIAT targets. Our data suggests that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation.

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