Ikaros-induced gene expression chages upon Ikaros re-expression in the ILC87 Ikaros-deficient tumor cell line
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE72801 | GEO | 2015/11/03
SECONDARY ACCESSION(S): PRJNA295086
REPOSITORIES: GEO
Similar Datasets
Project description:We used microarrays to analyze gene expression changes in the Ikaros null ILC87 T cell tumor line after re-expression of Ikaros. ILC87 cells were transduced to stably express the 4-hydroxytamoxifen-inducible (4OHT) Ikaros1-ER fusion protein. ILC87-Ik1-ER cells were treated with mock (EtOH) or 4OHT for 1 day and the global gene expression changes were assessed by microarray analysis.
2015-11-03 | E-GEOD-72801 | biostudies-arrayexpress
Project description:The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1
2013-11-30 | GSE51350 | GEO
Project description:The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1 The mouse BH1 pre-B cell line was transduced with retroviruses encoding Bcl2 and an Ikaros-estrogen receptor fusion protein. Doubly transduced cells were purified by FACS (BH1-Bcl2-Ik1ER). The transcriptome of these cells was analyzed at time 0, and after 6h and 24h of induction of Ikaros activity with 4-hydroxytamoxifen (4OHT) and/or withdrawal of IL-7. Samples from 2 independent experiments were analyzed (exp1 and exp2).
2013-11-30 | E-GEOD-51350 | biostudies-arrayexpress
Project description:Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. Our results identified novel Ikaros functions in the epigenetic regulation of gene expression: Ikaros directly regulates de novo formation and depletion of enhancers, as well as de novo formation of active enhancers and activation of poised enhancers; Ikaros directly induces the formation of super-enhancers; and Ikaros demonstrates pioneering activity by directly regulating chromatin accessibility. Dynamic analyses demonstrate the long-lasting effect of Ikaros DNA binding on enhancer activation, de novo formation of enhancers and super-enhancers, and chromatin accessibility. Ikaros induces profound, global re-distribution of HDAC1 via recruitment of HDAC1 to promoter and enhancer regions of different target genes. Expression analysis identified a large number of novel signaling pathways that are directly regulated by Ikaros and Ikaros-induced enhancers, and that are responsible for the cessation of proliferation and induction of T-cell differentiation in T-ALL cells.
2019-03-31 | GSE126391 | GEO
Project description:Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. Our results identified novel Ikaros functions in the epigenetic regulation of gene expression: Ikaros directly regulates de novo formation and depletion of enhancers, as well as de novo formation of active enhancers and activation of poised enhancers; Ikaros directly induces the formation of super-enhancers; and Ikaros demonstrates pioneering activity by directly regulating chromatin accessibility. Dynamic analyses demonstrate the long-lasting effect of Ikaros DNA binding on enhancer activation, de novo formation of enhancers and super-enhancers, and chromatin accessibility. Ikaros induces profound, global re-distribution of HDAC1 via recruitment of HDAC1 to promoter and enhancer regions of different target genes. Expression analysis identified a large number of novel signaling pathways that are directly regulated by Ikaros and Ikaros-induced enhancers, and that are responsible for the cessation of proliferation and induction of T-cell differentiation in T-ALL cells.
2019-03-31 | GSE126568 | GEO
Project description:Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. Our results identified novel Ikaros functions in the epigenetic regulation of gene expression: Ikaros directly regulates de novo formation and depletion of enhancers, as well as de novo formation of active enhancers and activation of poised enhancers; Ikaros directly induces the formation of super-enhancers; and Ikaros demonstrates pioneering activity by directly regulating chromatin accessibility. Dynamic analyses demonstrate the long-lasting effect of Ikaros DNA binding on enhancer activation, de novo formation of enhancers and super-enhancers, and chromatin accessibility. Ikaros induces profound, global re-distribution of HDAC1 via recruitment of HDAC1 to promoter and enhancer regions of different target genes. Expression analysis identified a large number of novel signaling pathways that are directly regulated by Ikaros and Ikaros-induced enhancers, and that are responsible for the cessation of proliferation and induction of T-cell differentiation in T-ALL cells.
2019-03-31 | GSE126567 | GEO
Project description:The Ikaros zink finger transcription factor is a critical regulator of the hematopietic system, and plays an important role in the regulation of the development and function of several blood cell lineages. We used microarrays to characterize how Ikaros deficieny affects global transcription in the hematopoietic stem and progenitor cells from wild-type and Ikaros mutant mice.
2015-11-03 | GSE61147 | GEO
Project description:The Ikaros zink finger transcription factor is a critical regulator of the hematopietic system, and plays an important role in the regulation of the development and function of several blood cell lineages. We used microarrays to characterize how Ikaros deficieny affects global transcription in the hematopoietic stem and progenitor cells from wild-type and Ikaros mutant mice. lin- Sca1+ c-Kit+ (LSK) cells, that contains the hematopoietic stem cells and the multipotent progenitor cells, were sorted by FACS from the bone marrow of 6-7 weeks old WT and IkL/L mutant mice. Total RNA extracted from these cells was subjected to transcriptome analysis.
2015-11-03 | E-GEOD-61147 | biostudies-arrayexpress
Project description:The mouse Ikaros-deficient thymic lymphoma cell line T29 was transduced with an empty retrovirus (MigR1) or a retrovirus expressing an fusion proein between Ikaros1 and the ligand binding domain of the estrogen receptor. Cells trreated with ethanol or 4-hydroxy-tamoxyfen (4OHT) for 24h were profiled. We used expression of an inducible ersion of the Ikaros protein in an Ikaros-deficient cell line to identify Ikaros-regulated genes
2013-04-17 | E-GEOD-46088 | biostudies-arrayexpress
Project description:We found that CD4+ T cells require Ikaros to promote IL-17 production when cultured in Th17 conditions. To understand why Ikaros null T cells do not produce IL-17, we analyzed the transcriptome of WT vs. Ikaros null naive CD4+ T cells both resting (day 0) or activated with anti-CD3 plus anti-CD28 antibodies, IL-6, TGFb1 and neutralizing anti-IFNg and anti-IL-4 antibodies (Th17 condition) for 1 or 2 days. Samples from 3 independent experiments were analyzed.
2021-04-26 | GSE133878 | GEO