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Defining AP4-regulated gene expression programs in pro/pre-B cells overexpressing c-MYC

ABSTRACT: Defining AP4-regulated gene expression programs in pro/pre-B cells overexpressing c-MYC

PROVIDER: PRJNA551667 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9621090.fastq.gz	Fastqsanger.gz
	SRR9621100.fastq.gz	Fastqsanger.gz
	SRR9621110.fastq.gz	Fastqsanger.gz
	SRR9621120.fastq.gz	Fastqsanger.gz
	SRR9621130.fastq.gz	Fastqsanger.gz

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Similar Datasets

Defining AP4-regulated gene expression programs in pro/pre-B cells overexpressing c-MYC

Project description:A hallmark feature of adaptive immune cells is their capacity for rapid cell proliferation required for producing and expanding cells with a diverse repertoire of antigen receptor and amplification of antigen-specific receptors. While proliferation is beneficial for host protection from infection and cancers, it inevitably elevates the risk of oncogenic transformation. Developing lymphocytes, as well as B cells in the germinal center (GC), are considered tumor-prone due to additional genomic insults from physiological antigen receptor gene rearrangement and editing. However, oncogenic transformation of lymphocytes is relatively rare, perhaps owing to an intrinsic, tumor-suppressive program. Here, we show that c-MYC not only facilitates rapid cell proliferation but, unexpectedly, also engages a counteracting tumor suppressive program through its downstream transcription factor, AP4. Haploinsufficiency for AP4 dramatically accelerates MYC-driven tumorigenesis in a B cell-intrinsic manner. At a mechanistic level, AP4 suppresses Erg, which is required for B cell development but also oncogenic, in MYC+ developing B cells, and thus AP4 restricts simultaneous expression of multiple oncogenic factors during B cell development. Thus, c-MYC has dual action that permit proliferative expansion of B cell precursors, while concurrently safeguarding against their transformation via engagement of an AP4-dependent, tumor-suppressive program.

2021-06-19 | GSE133514 | GEO

Defining AP4- and MYC-regulated gene expression programs in germinal center B cells during cyclic re-entry

Project description:B cells diversify and affinity-mature their antigen receptor repertoire in germinal centers (GC). GC B cells receive help signals during transient interaction with T cells, yet it remains unknown how these transient T-B interactions sustain the subsequent proliferative program of selected B cells. Here we show that the transcription factor AP4 is required for sustained GC B cell proliferation and subsequent establishment of a diverse and protective antibody repertoire. AP4 is induced by c-MYC during the T-B interactions and maintained by T cell-derived IL-21. B cell-specific deletion of AP4 resulted in reduced GC sizes and somatic hypermutation and a failure to control chronic viral infection. These results indicate that AP4 integrates T cell-mediated selection and sustained expansion of GC B cells for humoral immunity. Splenic B cells activated with anti-IgM and CD40L in vitro and germinal center B cells sorted from C57BL/6 mice eight days after immunization with sheep red blood cells (SRBCs) were obtained and genome-wide occupancy of c-MYC, AP4 and active histone marks was profiled by chromatin immunoprecipitation and high-throughput sequencing. Gene expression in MYCâAP4â LZ, MYC+AP4+ LZ, AP4+ DZ, and APâ DZ GC B cells from SRBC-immunized AP4-mCherry / c-MYC-GFP dual reporter mice was profiled by RNA-seq.

2016-08-23 | E-GEOD-80669 | biostudies-arrayexpress

Defining AP4- and MYC-regulated gene expression programs in germinal center B cells during cyclic re-entry

2016-08-23 | GSE80669 | GEO

Spatial organization, chromatin accessibility and gene-regulatory programs defining sensory neurons

Project description:Spatial organization, chromatin accessibility and gene-regulatory programs defining sensory neurons

| PRJNA1213725 | ENA

Gene expression analysis of cMyc-deficient CD8 T cells retrovirally overexpressing cMyc or AP4

2014-07-13 | GSE58079 | GEO

Autocrine vitamin D signaling switches off pro-inflammatory programs of Th1 cells

Project description:Autocrine vitamin D signaling switches off pro-inflammatory programs of Th1 cells

| PRJNA647352 | ENA

CAR-macrophages for the Treatment of HER2 Overexpressing Solid Tumors

Project description:Phase 1, first-in-human, open label study of CAR macrophages in HER2 overexpressing solid tumors.

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Unveiling IRF4-steered regulation of context-dependent effector programs in CD4+ T cells under Th17- and Treg-skewing conditions

Project description:The transcription factor IRF4 is crucial for the fate determination of pro-inflammatory T helper (Th)17 and the functionally opposing group of immunomodulatory regulatory T (Treg) cells. However, molecular mechanisms of how IRF4 steers diverse transcriptional programs in Th17 and Treg cells are far from being definitive. To unveil IRF4-driven lineage determination, we integrated data derived from affinity-purification and full mass spectrometry-based proteome analysis with chromatin immune precipitation sequencing. This allowed the characterization of subtype-specific molecular programs and the identification of IRF4 interactors in the Th17/Treg context. Our data reveal that IRF4-interacting transcription factors are recruited to IRF composite elements for the regulation of cell type-specific transcriptional programs as exemplarily demonstrated for FLI1, which in cooperation with IRF4 promotes Th17-specific gene expression. Inhibition of FLI1 markedly impaired Th17-differentiation. The present ‘omics’ dataset provides a valuable resource for studying IRF4-mediated gene regulatory programs in pro- and anti-inflammatory immune responses.

2025-03-05 | PXD060137 | JPOST Repository

An eRNA Transcription Checkpoint For Diverse Signal-dependent Enhancer Activation Programs [PRO-Seq]

Project description:An eRNA Transcription Checkpoint For Diverse Signal-dependent Enhancer Activation Programs [PRO-Seq]

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Gene expression analysis of cMyc-deficient CD8 T cells retrovirally overexpressing cMyc or AP4

Project description:To determine functional overlap between cMyc and AP4 in CD8+ T cell priming, we retrovirally expressed cMyc or AP4 in cMyc-deficient CD8+ T cells and examined gene expression after activation. Naive CD8+ T cells from Myc conditional knockout mice with a tamoxifen inducible Cre transgene were retrovirally transduced with Myc or AP4 followed by a treatment with 4-hydroxytamoxifen in the presence of IL-7 for 2 days. RNA was harvested 48 hours after restimulation of transduced cells with anti-CD3 antibody and gene expression was compared by microarray. CD8+ T cells from littermate wildtype mice that were transduced with an empty retrovirus were used as control.

2014-07-13 | E-GEOD-58079 | biostudies-arrayexpress

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