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The HES1 effects on TCL cells

ABSTRACT: The HES1 effects on TCL cells

PROVIDER: PRJNA821084 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18516657_1.fastq.gz	Fastqsanger.gz
	SRR18516657_2.fastq.gz	Fastqsanger.gz
	SRR18516658_1.fastq.gz	Fastqsanger.gz
	SRR18516658_2.fastq.gz	Fastqsanger.gz
	SRR18516659_1.fastq.gz	Fastqsanger.gz

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The HES1 effects on TCL cells

Project description:This study investigated the effects of HES1 depletion on TCL cells with RNA expression profile of two ALK+ TCL cells by Highthrough sequencing

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Hes1 and Glucocorticoid Signaling in Bone Sarcoma Cells

Project description:To investigate the role of HES1 during glucocorticoid signaling in bone sarcoma cells (U2OS-GR cells) , we employed whole-genome microarray expressions in mRNA extracted from control U2OS-GR and Hes1-overexpressed U2OS-GR cells.

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Hes1 and Glucocorticoid Signaling in Bone Sarcoma Cells

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Gene expression profile upon IL-22 stimulation, forced expression of Hes1, or IL-22 stimulation under forced expression of Hes1, in human colon carcinoma-derived LS174T cells

Project description:A human colon carcinoma-derived cell line LS174T was modified to overexpress Hes1, a bHLH-type transcription factor, upon doxycycline addition (designated as LS174T-tetON-Hes1 cells), using the T-rex system (Invitrogen). We have previously shown that these cells can overexpress Hes1 under the control of CMV promoter (Zheng et al, Inflamm Bowel Dis, 17;2251-2260, 2011), and the amont of the overexpressed Hes1 protein reaches to the maximal level in early as 3 hours from doxycycline addition (100ng/ml), which persists for up to 24 hours. In the present experiment, LS174T-tetON-Hes1 cells were treated with recombinant human IL-22 (20ng/ml) alone, doxycycline alone (100ng/ml), co-treated by both IL-22 and doxycycline, or left untreated (Control) for 24 hours, and subjected for analysis. Experiment was done using a modified sub-line of LS174T cell (LS174T-tetON-Hes1 cells), in which overexpression of Hes1 can be induced by a Doxycycline dependent manner.

2013-10-01 | GSE43012 | GEO

Genome-wide maps of HES1 binding-site in human chondrogenic cell.

Project description:Notch signaling modulates skeletal formation and osteoarthritis (OA) development through induction of catabolic factors. Here we examined functional roles of Hes1, the representative downstream transcription factor of Notch signaling, during these processes. Chromatin immunoprecipitation-sequencing (ChIP-seq) identified resposive elements of Hes1 around gene loci of Mmp13 and Adamts5, which were catabolic enzymes of cartilage matrix. Examination of HES1 binding site in human chondrogenic SW1353 cells.

2014-08-02 | E-GEOD-60006 | biostudies-arrayexpress

Gene expression profile upon IL-22 stimulation, forced expression of Hes1, or IL-22 stimulation under forced expression of Hes1, in human colon carcinoma-derived LS174T cells

2013-10-01 | E-GEOD-43012 | biostudies-arrayexpress

Gene expression alteration in chondrocyte by HES1 overexpression

Project description:To investigate target molecules of HES1, we transduced GFP or HES1 into mouse chondrocyte cell line ATDC5, and performed the microarray analysis. HES1 overexpression increased inflammation-related genes including Il6 and Il1rl1. We established stable ATDC5 cells overexpressing GFP or HES1 by lentiviral transduction. We harvested mRNA from these cells, and performed microarray analysis.

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Expression analysis of common myeloid progenitors (CMPs) expressing Hes1

Project description:High levels of Hes1 expression are frequently found in BCR-ABL-positive chronic myelogenous leukemia in blast crisis (CML-BC). In mouse bone marrow transplantation (BMT) models, co-expression of BCR-ABL and Hes1 induces CML-BC–like disease; however the underlying mechanism remained elusive. Here, based on gene expression analysis, we show that MMP-9 is upregulated by Hes1 in common myeloid progenitors (CMPs). Analysis of promoter activity demonstrated that Hes1 upregulated MMP-9 by activating NF-kB. Analysis of 20 samples from CML-BC patients showed that MMP-9 was highly expressed in three, with two exhibiting high levels of Hes1 expression. Interestingly, MMP-9 deficiency impaired the cobblestone area-forming ability of CMPs expressing BCR-ABL and Hes1 that were in conjunction with a stromal cell layer. In addition, these CMPs secreted MMP-9, promoting the release of soluble Kit-ligand (sKitL) from stromal cells, thereby enhancing proliferation of the leukemic cells. In accordance, mice transplanted with CMPs expressing BCR-ABL and Hes1 exhibited high levels of sKitL as well as MMP-9 in the serum. Importantly, MMP-9 deficiency impaired the development of CML-BC–like disease induced by BCR-ABL and Hes1 in mouse BMT models. The present results suggest that Hes1 promotes the development of CML-BC, partly through MMP-9 upregulation in leukemic cells.

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RNA-seq of Pdx1-GFP+ sorted E10.5, wildtype and Hes1-/-. Neurog3-dependent Pancreas Dysgenesis Causes Ectopic Pancreas in Hes1 Mutants

Project description:RNA-seq of FACS Sorted E10.5 Pdx1-GFP+ of genotypes wildtype and Hes1-/-. Summary statement The developmental mechanisms that cause ectopic pancreas are poorly understood. We show that aberrant dorsal pancreas morphogenesis in Hes1 mutants leads to ectopic pancreas depending on the pro-endocrine gene Neurog3. Abstract Mutations in Hes1, a target gene of the Notch signalling pathway, lead to ectopic pancreas by a poorly described mechanism. Here we use genetic inactivation of Hes1 combined with lineage tracing in mouse embryos to reveal an endodermal requirement for Hes1 and that most ectopic pancreas tissue is derived from the E8.5 dorsal pancreas primordium. RNA-seq data from sorted E10.5 Pdx1-GFP+ cells from Hes1+/+ and Hes1−/− suggested that upregulation of endocrine lineage genes in Hes1−/− embryos was the major defect in the endoderm and accordingly early pancreas morphogenesis was normalised and the ectopic pancreas phenotype suppressed in Hes1−/−Neurog3−/− embryos. Analysis of other Notch pathway mutants uncovered a total depletion of progenitors in Mib1 deficient dorsal anlage, which was replaced by an anterior Gcg+ extension. Together, our results demonstrate that aberrant morphogenesis is the cause of ectopic pancreas and that a part of the endocrine differentiation program is mechanistically involved in the dysgenesis. Our results suggest that the ratio of endocrine lineage to progenitor cells is important for morphogenesis and that a strong endocrinogenic phenotype without complete progenitor depletion as seen in Hes1 mutants provokes an extreme dysgenesis that causes ectopic pancreas.

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Gene expression alteration in chondrocyte by HES1 overexpression

2015-03-02 | GSE60737 | GEO