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ChIP-seq studies of Th17 cells in Malat1 KO and WT mice

ABSTRACT: ChIP-seq studies of Th17 cells in Malat1 KO and WT mice

PROVIDER: PRJNA878784 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21502100.fastq.gz	Fastqsanger.gz
	SRR21502101.fastq.gz	Fastqsanger.gz
	SRR21502102.fastq.gz	Fastqsanger.gz
	SRR21502103.fastq.gz	Fastqsanger.gz
	SRR21562251.fastq.gz	Fastqsanger.gz

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Transcriptomic studies of mouse naïve and Th17 cell from wildtype or Malat1 deficient background

Project description:Long non-coding RNAs (lncRNAs) are critical regulators of mammalian gene programs. Metastasis Associated Lung Adenocarcinoma Transcript 1 (Malat1) is the most abundant lncRNA expressed in intestinal Th17 cells critical for maintaining tissue homeostasis and regulating local inflammation. Here, we report that Malat1 negatively regulates IL-17A and IL-17F productions in intestinal Th17 cells during colitis and contributes to local inflammation. Global RNA interactions with DNA by deep sequencing (GRID-seq) coupled with transcriptomic studies revealed Malat1 is recruited to the Il17a-Il17f super enhancer in Th17 cells, and regulates Il17a-Il17f transcription.

2024-12-31 | GSE190561 | GEO

Differential Gene expression in the mouse mammary tumors of PyMT-Malat1 wild-type (WT), PyMT-Malat1 knockout (KO) and PyMT-Malat1 knockout with Malat1 transgene expression (TG)

Project description:Previously, lncRNA Malat1 knockout mice were generated by insertional inactivation. By crossing this line to MMTV-PyMT mammary tumor mouse model, we produced PyMT;Malat1 wild-type (WT) and PyMT;Malat1 knockout (KO). Furthermore, we generated Malat1 transgenic mice by targeting ROSA26 locus and bred them to PyMT;Malat1 knockout mice to produce Malat1-rescued PyMT;Malat1 knockout;Malat1 transgenic animals (TG). Using mammary tumors from the three groups of animals, we performed RNA-Seq analysis to identify differentially up-regulated genes in KO tumors to find novel target genes of YAP-TEAD pathway.

2018-09-18 | GSE110239 | GEO

GRID-seq studies of mouse naïve and culture Th17 cells from wildtype mice

2024-12-31 | GSE190560 | GEO

Transcriptomic studies of mouse naïve and Th17 cell from wildtype or Malat1 deficient background

Project description:Transcriptomic studies of mouse naïve and Th17 cell from wildtype or Malat1 deficient background

| PRJNA787542 | ENA

Differential Gene expression in the mouse mammary tumors of PyMT-Malat1 wild-type (WT), PyMT-Malat1 knockout (KO) and PyMT-Malat1 knockout with Malat1 transgene expression (TG)

Project description:Differential Gene expression in the mouse mammary tumors of PyMT-Malat1 wild-type (WT), PyMT-Malat1 knockout (KO) and PyMT-Malat1 knockout with Malat1 transgene expression (TG)

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Effects of the long noncoding RNA Malat1 on gene expression [Mouse430_2]

Project description:Malat1 is an abundant long noncoding RNA that localizes to nuclear bodies known as nuclear speckles, which contain a distinct set of pre-mRNA processing factors. Previous in vitro studies have demonstrated that Malat1 interacts with pre-mRNA splicing factors, including the serine- and arginine-rich (SR) family of proteins, and regulates a variety of biological processes, including cancer cell migration, synapse formation, cell cycle progression, and responses to serum stimulation. To address the physiological function of Malat1 in a living organism, we generated Malat1-KO (KO) mice using homologous recombination. Unexpectedly, the Malat1-KO mice were viable and fertile, showing no apparent phenotypes. Nuclear speckle markers were also correctly localized in cells that lacked Malat1. However, the cellular levels of another long noncoding RNA, Neat1, which is an architectural component of nuclear bodies known as paraspeckles, were downregulated in a particular set of tissues and cells lacking Malat1. To address if the the absence of Malat1 affects the expression of other genes, including other long noncoding RNA, microarrays were used to study the impact of knocking-out Malat1 on global gene expression in mouse embryonic fibroblasts (MEFs). MEFs were prepared from E13.5 mouse embryos from wildtype and Malat1 knock-out mice. RNA harvested from these cells were hybridized to Affymetirx mouse gene expression array.

2012-06-24 | E-GEOD-37705 | biostudies-arrayexpress

Effects of the long noncoding RNA Malat1 on gene expression [MoEx-1_0-st]

Project description:Malat1 is an abundant long noncoding RNA that localizes to nuclear bodies known as nuclear speckles, which contain a distinct set of pre-mRNA processing factors. Previous in vitro studies have demonstrated that Malat1 interacts with pre-mRNA splicing factors, including the serine- and arginine-rich (SR) family of proteins, and regulates a variety of biological processes, including cancer cell migration, synapse formation, cell cycle progression, and responses to serum stimulation. To address the physiological function of Malat1 in a living organism, we generated Malat1-KO (KO) mice using homologous recombination. Unexpectedly, the Malat1-KO mice were viable and fertile, showing no apparent phenotypes. Nuclear speckle markers were also correctly localized in cells that lacked Malat1. However, the cellular levels of another long noncoding RNA, Neat1, which is an architectural component of nuclear bodies known as paraspeckles, were downregulated in a particular set of tissues and cells lacking Malat1. To address if the absence of Malat1 affects the expression of other genes, including other long noncoding RNA, microarrays were used to study the impact of knocking-out Malat1 on global gene expression in hippocampal neurons. Hippocampi were dissected from two sets of wildtype and Malat1 knock-out mice and RNA from these neurons were hybridized to Affymetix mouse exon array. Individual animals from each pairs of wildtype and knock-out are littermates.

2012-06-24 | E-GEOD-37706 | biostudies-arrayexpress

Transcription profiles of fate mapped IL17aiCre+flox/stop/flox-YFP+ TH17 cells, CD44intCD27+ TH17 cells and CD44hiCD27- TH17 cells from WT or Raptor-ko (flox/flox) mice after immunization with Myelin Oligodendrocyte Glycoprotein (MOG)

Project description:Mechanisms governing memory responses in IL-17 secreting CD4+ T cells (TH17), especially in autoimmune disorders, remain poorly understood. TH17 cells play pleiotropic roles in autoimmunity and tissue inflammation and are characterized by inherent plasticity, although how plasticity is regulated remains elusive. We investigated the transcriptional profiles of fate mapped (IL17aiCre-flox/stop/flox-YFP) TH17 cells and WT and Raptor-ko (flox/flox) TH17 cells (both IL17aiCre-flox/stop/flox-YFP) as well as sorted within CD27+ and CD27- subsets of WT in experimental autoimmune encephalomyelitis, a human model for human multiple sclerosis. We used microarrays to compare the global transcription profiles of YFP+ (IL17aiCre-flox/stop/flox-YFP) fate mapped TH17 cells as well as CD27+ and CD27- subsets of CD44+ fate mapped TH17 cells from draining lymph nodes on day 9 after immunization with Myelin oligodendrocyte glycoprotein from WT and IL17aCre-Raptor-flox/flox mice.

2019-03-20 | GSE107521 | GEO

ChIP-seq studies of Th17 cells in Malat1 KO and WT mice

Project description:Chromatin immunoprecipitation (ChIP) was performed in biological replicates. For H3K27me3 ChIP assays, cells were cross-linked with 1% (vol/vol) formaldehyde. For SUZ12 and EZH2 ChIP assays, cells were cross-linked with 2 mM disuccinimidyl glutarate (DSG) and 1% (vol/vol) formaldehyde.

2024-12-31 | GSE213014 | GEO

Population transcriptional profiling of KO or WT cells,, differentiated in vitro for 48-96h towards Th17 cells

Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Population transcriptional profiling of KO or WT cells,, differentiated in vitro for 48-96h towards Th17 cells

2015-11-20 | E-GEOD-75104 | biostudies-arrayexpress

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