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The HES1 effects on TCL cells

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE199658 | GEO | 2022/05/24

REPOSITORIES: GEO

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The HES1 effects on TCL cells

Project description:The HES1 effects on TCL cells

| PRJNA821084 | ENA

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.

2018-08-20 | E-MTAB-6890 | biostudies-arrayexpress

Expression of SUDHL-1 cell line treated by ALK inhibitors

Project description:In this study we compared the effects of ALK inhibitor on the gene expression, activation of cell signaling pathways, and functional properties of cells derived from a patient with Anaplastic Large Cell Lymphoma. we used microarrays to map the genome-wide gene expression patterns in ALK+TCL cells in response to ALK inhibition. The ALK+TCL Sudhl-1 cell line was treated in triplicates with the ALK inhibitor, CEP-14083, or the compound's solvent for 6 h. The isolated RNA was reverse-transcribed, biotin-labeled, and hybridized to the U133 Plus 2.0 array chips (Affymetrix). Microarray data were normalized using the MAS5 algorithm and analyzed using Partek GS (Partek).

2013-10-31 | E-GEOD-50803 | biostudies-arrayexpress

Effects of ALK inhibitory treatment with alectinib in glioblastoma cells

Project description:Anaplastic lymphoma kinase (ALK) is expressed in around 60% of glioblastomas and conveys tumorigenic function. Therefore, ALK inhibitory strategies with alectinib were investigated in glioblastoma cells. We demonstrated that alectinib inhibited proliferation and clonogenicity of ALK expressing glioblastoma initiating cells, whereas cells without ALK expression or after ALK depletion via knockdown showed primary resistance against alectinib. The aim of this analysis was to investigate molecular mechanisms of alectinib mediated treatment effects in the ALK expressing S24 cells, which represent a primary glioblastoma cell culture, and after knockdown of ALK.

2019-11-09 | GSE140145 | GEO

Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL3]

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Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL2]

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Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL1; T8ML1]

Project description:To study differential gene expression of TCLs upon TCR signaling, three TCL primary cells and one TCL cell line T8ML1 were chosen for this study. The prmiary TCL cells consist of TCL1 and TCL2 (sezary patients) and TCL3 (PTCL, NOS patient). The TCR signaling was engaged by anti-CD3/CD28 treatment in vitro. The TCL cells were treated without/with anti-CD3/CD28 for different time periods in vitro in cell culture. The total RNA was isolated from the TCLs and subjected to affimetry microarray (GPL17692) analysis. The differential gene expression of individual TCL was identified as well as a set of common genes invloved in TCR signaling in TCLs. The subject for this study includes pirmary cells isolated from three TCL patients [two sezary patients (TCL1 & TCL2) and one PTCL, NOS patient (TCL3)] and cells from a TCL cell line (T8ML1). The purity of isolated primary cells is >93% as idnetified by flow cytometry. The TCLs were treated with/without anti-CD3/CD28 for different time points, with 2-3 replicates for each time point. Gene expression value was presented as Log2 transformed. Differntial expressed genes were identified by ∆log2x>1 in comparison to no anti-CD3/CD28 treatment.

2017-02-10 | GSE77875 | GEO

Expression of SUDHL-1 cell line treated by ALK inhibitors

2013-10-31 | GSE50803 | GEO

ALK effection analysis on T-lymphocyte cells

2024-11-01 | GSE217889 | GEO

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.

2014-01-21 | GSE52727 | GEO

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