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Gene expression analysis of Cbfb-deficient LSK and GMP

ABSTRACT: Runx/Cbfb heterodimers play important roles in the development of hematopoietic cells in mouse embryos and adults. In order to identify genes that are regulated by Runx/Cbfb, we purified Lin– c-kit+ Sca1+ (LSK) cells and Lin– c-kit+ Sca1– CD16/32+ (GMP) cells from Vav1-iCre x Cbfb(F/F) and Vav1-iCre x Cbfb(F/+) mice and profiled gene expression using microarray.

ORGANISM(S): Mus musculus

PROVIDER: GSE55227 | GEO | 2014/04/05

SECONDARY ACCESSION(S): PRJNA238934

REPOSITORIES: GEO

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Gene expression analysis of Cbfb-deficient LSK and GMP

Project description:Runx/Cbfb heterodimers play important roles in the development of hematopoietic cells in mouse embryos and adults. In order to identify genes that are regulated by Runx/Cbfb, we purified Lin– c-kit+ Sca1+ (LSK) cells and Lin– c-kit+ Sca1– CD16/32+ (GMP) cells from Vav1-iCre x Cbfb(F/F) and Vav1-iCre x Cbfb(F/+) mice and profiled gene expression using microarray. 200,000 LSK and GMP cells were purified separately from two 7 week old Vav1-iCre x Cbfb(F/F) mice and two Vav1-iCre x Cbfb(F/+) mice by cell sorting. The purity was higher than 98%. Total RNA was extracted using the NucleoSpin RNA XS kit (Macherey-Nagel), amplified using a PicoSL RNA amplification kit (Nugen) and biotinylated with Encore biotin module (Nugen). Labeled RNA was hybridized to Mouse Gene 1.0ST microarrays (Affymetrix) according to the manufacturer’s instruction.

2014-04-05 | E-GEOD-55227 | biostudies-arrayexpress

Mouse inv(16):TET2ko granulocyte macrophage progenitor (GMP) cells

Project description:inv(16)/Tet2-/- GMPs (Lin- Sca1- ckit+ CD41- FcgR+ CD150-) were FACS sorted as described in Supplementary Information (Reckzeh, K et al 2020) TET2 deficiency cooperates with CBFB-MYH11 to induce acute myeloid leukemia and represents an early leukemogenic event. Reckzeh, K et al.

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The effect of periodontitis - induced trained immunity on the epigenomic profile of mouse bone marrow LSK and GMP cells

Project description:Peripheral inflammation affects hematopoietic stem and progenitor cells (HSPCs) in the bone marrow and induce myeloid lineage skewing of the progenitor cells. In this study, we performed single cell ATAC-sequencing in LSK (Lin—Sca-1+cKit+ ) and GMP (Lin—c-Kit+Sca1—CD16/32+CD34+) cells to determine the impact of ligature-induced periodontitis (LIP) on the epigenomic profile of these BM cells.

2022-04-27 | GSE180025 | GEO

Transcription profiling of mouse Cbfb-deficient regulatory T cells

Project description:Gene expression profiles of Cbfb-deficient and control Treg cells were compared. Abstract: Naturally arising regulatory T (Treg) cells express the transcription factor FoxP3, which critically controls the development and function of Treg cells. FoxP3 interacts with another transcription factor Runx1 (also known as AML1). Here we showed that Treg cell-specific deficiency of Cbfβ, a cofactor for all Runx proteins, or that of Runx1, but not Runx3, induced lymphoproliferation, autoimmune disease, and hyper-production of IgE. Cbfb-deleted Treg cells exhibited impaired suppressive function in vitro and in vivo, with altered gene expression profiles including attenuated expression of FoxP3 and high expression of interleukin-4. The Runx complex bound to more than 3000 gene loci in Treg cells, including the Foxp3 regulatory regions and the Il4 silencer. In addition, knockdown of RUNX1 showed that RUNX1 is required for the optimal regulation of FoxP3 expression in human T cells. Taken together, our results indicate that the Runx1-Cbfβ heterodimer is indispensable for in vivo Treg cell function, in particular, suppressive activity and optimal expression of FoxP3. Experiment Overall Design: CD4+CD25hi cells, most of which were Foxp3+ Treg cells, were isolated from Cbfb-flox/flox: Foxp3-ires-Cre (n = 3) and control Cbfb-flox/wt: Foxp3-ires-Cre (n = 3) mice. Total RNA was extracted from those purified Cbfb-deficient or control Treg cells.

2009-09-25 | E-GEOD-18148 | biostudies-arrayexpress

CBFb Stabilizes HIV Vif to Counteract APOBEC3 at the Expense of RUNX1 Target Gene Expression [ChIP-seq]

Project description:The HIV-1 accessory protein Vif hijacks a cellular Cullin-RING ubiquitin ligase, CRL5, to promote degradation of the APOBEC3 (A3) family of restriction factors. Recently, the cellular transcription cofactor CBFb was shown to form a complex with CRL5-Vif and to be essential for A3 degradation and viral infectivity. We now demonstrate that CBFb is required for assembling a well-ordered CRL5-Vif complex by inhibiting Vif oligomerization and by activating CRL5-Vif via direct interaction. The CRL5-Vif-CBFb holoenzyme forms a welldeﬁned heterohexamer, indicating that Vif simultaneously hijacks CRL5 and CBFb. Heterodimers of CBFb and RUNX transcription factors contribute toward the regulation of genes, including those with immune system functions. We show that binding of Vif to CBFb is mutually exclusive with RUNX heterodimerization and impacts the expression of genes whose regulatory domains are associated with RUNX1. Our results provide a mechanism by which a pathogen with limited coding capacity uses one factor to hijack multiple host pathways. Identification of RUNX1 binding sites in the Jurkat cell line

2013-01-17 | E-GEOD-42575 | biostudies-arrayexpress

CBFb Stabilizes HIV Vif to Counteract APOBEC3 at the Expense of RUNX1 Target Gene Expression [gene expression]

Project description:The HIV-1 accessory protein Vif hijacks a cellular Cullin-RING ubiquitin ligase, CRL5, to promote degradation of the APOBEC3 (A3) family of restriction factors. Recently, the cellular transcription cofactor CBFb was shown to form a complex with CRL5-Vif and to be essential for A3 degradation and viral infectivity. We now demonstrate that CBFb is required for assembling a well-ordered CRL5-Vif complex by inhibiting Vif oligomerization and by activating CRL5-Vif via direct interaction. The CRL5-Vif-CBFb holoenzyme forms a wellde?ned heterohexamer, indicating that Vif simultaneously hijacks CRL5 and CBFb. Heterodimers of CBFb and RUNX transcription factors contribute toward the regulation of genes, including those with immune system functions. We show that binding of Vif to CBFb is mutually exclusive with RUNX heterodimerization and impacts the expression of genes whose regulatory domains are associated with RUNX1. Our results provide a mechanism by which a pathogen with limited coding capacity uses one factor to hijack multiple host pathways. Analysis of Vif-dependent effects on gene expression in Jurkats when cells are activated for 4 or 6 hours with PMA and PHA

2013-01-17 | E-GEOD-42574 | biostudies-arrayexpress

CBFb Stabilizes HIV Vif to Counteract APOBEC3 at the Expense of RUNX1 Target Gene Expression [ChIP-seq]

2013-01-17 | GSE42575 | GEO

CBFb Stabilizes HIV Vif to Counteract APOBEC3 at the Expense of RUNX1 Target Gene Expression [gene expression]

2013-01-17 | GSE42574 | GEO

Mx-Cre mediated deletion of SRF in murine hematopoietic LSK (Lin-Sca1+c-Kit+) cells

Project description:Analysis of hematopoietic LSK(Lin-Sca1+c-Kit+) cells lacking the Serum response factor (SRF) gene. Results provide insight into the role of SRF in regulating genetic programs important for hematopoietic stem cell development

2010-08-12 | GSE23556 | GEO

Gene expression differences between leukemic cells from Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M mice by microarray

Project description:Results showed that Chd7 deficiency delay Cbfb-MYH11 induced leukemia, to explore the mechanism, We also performed microarray analysis on c-Kit+ leukemic cells to determine gene expression differences between Mx1-Cre, Cbfb+/56M and Chd7f/f, Mx1-Cre, Cbfb+/56M leukemic cells.

2018-02-14 | GSE103367 | GEO

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