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Identification of Myc-dependent and -independent Notch2 signatures in marginal zone B cells.

ABSTRACT: Identification of Myc-dependent and -independent Notch2 signatures in marginal zone B cells.

PROVIDER: PRJNA1148917 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30273200.fastq.gz	Fastqsanger.gz
	SRR30273201.fastq.gz	Fastqsanger.gz
	SRR30273202.fastq.gz	Fastqsanger.gz
	SRR30273203.fastq.gz	Fastqsanger.gz
	SRR30273172.fastq.gz	Fastqsanger.gz

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Identification of Myc-dependent and -independent Notch2 signatures in marginal zone B cells.

Project description:Marginal zone (MZ) B cells leverage Notch2 signals to attain rapid differentiation responses and positional cues with in the spenic environment. While it is known that a major player in Notch2 signaling in MZ B cells is the proto-oncogene Myc, it is not clear to what extent MZ B cells use Notch2 signals in Myc-independent manner. In this study we conditinally and inducibly deleted Myc in mature B cells and then used in vivo delivery of anti-Notch2 antibodies to separated Myc-dependent and -independent Notch2 signaling in MZ B cells.

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Transcriptomic analyis follicular and marginal zone B ells after in vivo Notch2 blockade.

Project description:Marginal zone B cells which make rapid mitosis-independent plasma cell responses are dependent on Notch2 signaling for their generation and maintenance. In order to determine the effect of ongoing Notch signaling on the maintenance of the MZ transcriptome, we performed RNA-seq on MZ and follicular B cells after 12, 24 and 48 hours of in vivo Notch2 antibody blockade

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Marginal zone B cells leverage the Notch2-Myc-mTORC1 signaling axis to achieve division independent plasma cell differentiation.

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Marginal zone B cells receive robust Notch2 signals within the B cell follicle in the absense of S1pr1 signaling.

Project description:Marginal zone (MZ) B cells have innate-like response characteristics due to a unique ability receive and integrate Notch2 signals in the spleen. There is evidence showing MZ B cells receive these signals both in the marginal sinus and the B cell follicle. The relative strength and conservation of these Notch signals is not yet clear. Therefore, we generated mice in which S1pr1 is deleted in mature B cells. These mice have MZ B cells by phenotype but these cells are retained in the follicle and unable to transit to the marginal zone. In this experiment we examined the impact of Notch2 signaling in these cells and cre expressing control animals using in vivo anti-Notch2 antibody blockade followed by RNA-sequencing.

2024-10-18 | GSE274990 | GEO

Human splenic marginal zone precursors (MZP) differentiation into marginal zone B cells (MZB)through a Notch2 signalling pathway

Project description:RNA microarray profiling analysis was performed on different ex-vivo human splenic B cell subsets (M-^SNaM-oveM-^T, marginal zone precursors or M-^SMZPM-^T, marginal zone B cells orM-^T MZBM-^T, M-^SMTG+CD45+M-^T cells) and on M-^Sp27M-^T cells, corresponding to the fraction of MZP cells that differentiated into CD27-expressing cells after culture on OP9-hDLL1 cells cultured with OP9-hDLL1 cells that differentiated into CD27-expressing cells

2014-03-26 | E-MTAB-2244 | biostudies-arrayexpress

Notch2 Signaling Induces Trans-differentiation of Follicular to Marginal Zone B Cells

Project description:Notch2 Signaling Induces Trans-differentiation of Follicular to Marginal Zone B Cells

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Transcriptomic analyis follicular and marginal zone B ells after in vivo Notch2 blockade.

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Project description:This SuperSeries is composed of the following subset Series: GSE32231: Molecular characterization of Nodal marginal zone lymphoma [Gene Expression] GSE32232: microRNA-expression profile in a series of Nodal marginal zone lymphoma patients [miRNA expression] Refer to individual Series

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Molecular characterization of Nodal marginal zone lymphoma [Gene Expression]

Project description:Nodal marginal zone lymphoma (NMZL) is a small B cell neoplasm whose molecular pathogenesis is still essentially unknown and whose differentiation from other small B cell lymphomas is hampered by the lack of specific markers. We have analyzed gene expression, miRNA profile and copy number data from 15 NMZL cases. For comparison, 16 follicular lymphomas, 9 extranodal marginal zone lymphomas, 8 reactive lymph nodes and B-cell subtypes were included. The results were validated by qRT-PCR in an independent series including 61 paraffin-embedded NMZLs. NMZL signature showed an enriched expression of gene sets identifying interleukins, integrins, CD40, PI3K, NF-kB and TGF-Beta; and included genes expressed by normal marginal zone cells and memory B cells. The most highly overexpressed genes were SYK, TACI, CD74, CD82 and CDC42EP5. Genes linked to G2/M and germinal center were downregulated. Comparison of the gene expression profiles of NMZL and FL showed enriched expression of CHIT1, TGFB1 and TACI in NMZL, and BCL6, LMO2 and CD10 in FL. NMZL displayed increased expression of miR-221, miR-223 and let-7f, while FL strongly expressed miR-494. Our study identifies new candidate diagnostic molecules for NMZL and reveals survival pathways activated in NMZL. We have analyzed gene expression, miRNA profile and copy number data from 15 NMZL cases. For comparison, 16 follicular lymphomas, 9 extranodal marginal zone lymphomas, 8 reactive lymph nodes and B-cell subtypes were included. The results were validated by qRT-PCR in an independent series including 61 paraffin-embedded NMZLs

2011-09-20 | E-GEOD-32231 | biostudies-arrayexpress

BCR and TLR-induced IRF1 promotes T cell independent B cell responses by supporting Notch2 dependent Marginal Zone B cell development

Project description:The prototypic interferon (IFN)-inducible transcription factor, IRF1, not only controls expression of IFN genes but also regulates T cell and macrophage fate specification and function. We show that IRF1 expression in B cells is required for marginal zone B (MZB) cell development and T cell independent antibody responses [80% B6.129S2-Ighmtm1Cgn/J (MT) + B6.129S2-Irf1tm1Mak/J (Irf1-/-), B-Irf1-/- chimeras]. While IFNs can induce IRF1 expression in MZB precursors, IFN signaling is not required for MZB cell development [C57BL/6J (B6), B6.129S7-Ifngr1tm1Agt/J (Ifngr1-/-), B6(Cg)-Ifnar1tm1Agt/J (Ifnar1-/-)]. Instead, BCR and TLR signals, which influence MZB commitment, promote IRF1 expression and nuclear translocation in MZB cell precursors. In turn, IRF1 is required for Notch-dependent gene expression in transitional B cells and development of the MZB cell compartment. Thus, T independent MZB-driven antibody responses are regulated by BCR and TLR signals that initiate IRF1-dependent Notch programming of transitional B cells and subsequent commitment of these cells to the MZB lineage.

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