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Expression data from GFP-labeled c-Kit+ mouse APL cells and normal Lin-Sca-1-c-Kit+ mouse bone marrow cells

ABSTRACT: To characterize the differentially expressed genes between leukemic and normal myeloid progenitors

ORGANISM(S): Mus musculus

PROVIDER: GSE46434 | GEO | 2016/05/01

SECONDARY ACCESSION(S): PRJNA200341

REPOSITORIES: GEO

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Expression data from small intestinal Lin-c-Kit+Sca-1- cells and Lin-c-Kit-Sca-1- cells.

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Expression data from small intestinal Lin-c-Kit+Sca-1- cells and Lin-c-Kit-Sca-1- cells.

Project description:Small intestinal innate lymphoid cells (ILCs) are known to regulate intestinal epithelial cell homeostasis and to help prevent pathogenic bacterial infections, by producing IL-22. However, other functions of these cells and the lineal relationship between ILCs and lymphoid or myeloid cells have not been clear. We performed a global gene expression analysis to examine which genes are highly expressed by small intestinal ILCs (Lin-c-Kit+Sca-1- cells) compared with non-ILCs (Lin-c-Kit-Sca-1- cells). To examine the gene expression profiles of ILCs within the small intestinal lamina propria (LP), we isolated Lingeage (Lin)-c-Kit+Sca-1- cells [consisting of NKp46+ ILC22 (Lin-c-Kit+Sca-1-NKp46+ cells) and LTi-like ILC (Lin-c-Kit+Sca-1-CD4+ cells)] as the ILC population, and Lin-c-Kit-Sca-1- cells as the non-ILC population, from the small intestinal LP of 8 week-old mice by FACS, then compared the gene expression profiles between these two populations by microarray analysis.

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mRNA profiles of CD43++c-kit+, CD43+c-kit- and CD43-c-Kit- AML1-ETO9a murine leukemic bone marrow cells

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Project description:Notch activation is instrumental in the development of most T-cell acute lymphoblastic leukemia (T-ALL) cases, yet Notch mutations alone are not sufficient to recapitulate the full human disease in animal models. Using multiple in vivo and in vitro T-ALL models we here demonstrate that β-Catenin is essential for Notch-driven T-cell leukemic initiation. Transcriptome analyses of leukemic initiating cells revealed a switch in β-Catenin activity that was Notch-context dependent. Moreover, ChIP-seq coupled with RNA-Seq in human Notch-active T-ALL showed that leukemic β-Catenin was independent of canonical LEF/TCF partners, and instead depended on direct association with Notch or ZBTB33/Kaiso for gene activation. The functional relevance of this mechanism is exemplified by the MYC 3´enhancer that requires β-Catenin and Notch1 recruitment to induce MYC expression. Finally, we demonstrate that pharmacological inhibition of β-Catenin with PKF115-584 prevented and partially reverted leukemogenesis induced by active Notch1. These microarray data show the transcriptional activities of N1IC and β-Catenin in wild-type or leukemic initiating cell (LIC) contexts in N1IC-transduced adult Lineage-depleted BM cells.

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Expression data from cultured c-Kit+Sca-1+Lin- (KSL)cells

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Expression data from Sf3b1 heterozygous Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

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Expression data from cultured c-Kit+Sca-1+Lin- (KSL)cells

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