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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE274989 | GEO | 2024/10/18

REPOSITORIES: GEO

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Identification of Notch ligand useage by splenic B cells using Dll1 and Dll4 Notch ligand blockade.

Project description:Marginal zone (MZ) B cells leverage Notch2 signals to attain rapid differentiation responses and positional cues with in the spenic environment.To determine the likely molecular source of Notch2 signals we sought to block the Notch ligands delta-like ligand 1 (Dll1) and delta-like ligand 4 (Dll4) in wildtype mice using in-vivo treatment with monoclonal blocking antibodies. Splenic populations of MZ B cells and follicular B cells were sort purified after 12, 24 and 48 hours of blockade and analyzed by RNA-seq.

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Project description:The generation of marginal zone (MZ) B cells is a Notch2 dependent process. We observed that transdifferentiation of follicular (FO) B cells to an MZ-like phenotype is dependent on a lymphopenic environment. We therefore adoptively transftered congenically marked SJL.C20 (CD45.1) mature naive FO B cells into either lymphopenic Rag2-/- or intact C57BL6 (CD45.2) recipient mice and recovered and double sorted intermediate phenotype (MZ-FO) donor B cells at day 4 post transfer from Rag2-/- recipients or both MZ and FO phenotype donor B cells at day 8 post transfer from both recipient groups and performed RNA sequencing.

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Notch2 controls non-autonomous Wnt-signalling in chronic lymphocytic leukaemia

Project description:The Wnt-signalling pathway is one of the core de-regulated pathways in chronic lymphocytic leukemia (CLL), activated in a subset of patients by somatic coding mutations. Here we describe an alternative mechanism of Wnt-activation in malignant B cells, mediated by Notch2 activity in mesenchymal stromal cells (MSC) in the tumor microenvironment. We identified that tumor cells specifically induce and activate Notch2 in MSCs. Notch2 orchestrates the expression of target genes essential for the activation of canonical Wnt-signaling in CLL cells. Mechanistically, stromal Notch2 mediates the stabilization of â-catenin by inhibiting the activation of Gsk3-â in malignant B cells. Pharmacological inhibition of the Wnt-pathway mitigates microenvironment-mediated survival of malignant B cells in vitro. Similarly, inhibition of Notch-signaling impaired survival of CLL cells and disease engraftment in a PDX mouse model. Notch2 activation in the tumour microenvironment is a pre-requisite for the GSK3-â dependent activation of the canonical Wnt-signaling in tumor cells.

2018-09-19 | PXD010401 | Pride

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2011-12-31 | E-GEOD-31643 | biostudies-arrayexpress

(1) Effect of KLHL6 loss on the transcriptome in DLBCL upon NOTCH ligand stimulation. (2) Effect of KLHL6 and NOTCH2 loss on the transcriptome in DLBCL. (3) Effect of DLBCL-associated NOTCH2 mutants on the transcriptome in DLBCL.

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