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RNA sequencing comparing normal and premalignant EuMyc B220+ cells in Max WT and conditional Max KO mice

ABSTRACT: RNA sequencing comparing normal and premalignant EuMyc B220+ cells in Max WT and conditional Max KO mice

PROVIDER: PRJNA548948 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9304810_1.fastq.gz	Fastqsanger.gz
	SRR9304810_2.fastq.gz	Fastqsanger.gz
	SRR9304820_1.fastq.gz	Fastqsanger.gz
	SRR9304820_2.fastq.gz	Fastqsanger.gz
	SRR9304811_1.fastq.gz	Fastqsanger.gz

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RNA sequencing comparing normal and premalignant EuMyc B220+ cells in Max WT and conditional Max KO mice

Project description:The goal of this study was to compare expression profiles of B cells in the presence and absence of transcription factor MAX under normal and premalignant settings

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CUT&RUN comparing occupancy of MAX, MNT, MYC in MAX WT and KO B220+ cells

Project description:The goal of this study was to genomic occupancy of MAX, MNT, MYC and E2F1 in B cells in the presence and absence of transcription factor MAX Although MAX is regarded as an obligate dimerization partner for MYC, its function in normal development and neoplasia is poorly defined. We show that B-cell specific deletion of Max has a modest effect on B-cell development but completely abrogates E -Myc driven lymphomagenesis. While Max loss only affects a few hundred genes in normal B cells, it leads to the global downregulation of Myc-activated genes in premalignant E -Myc cells. We show that the balance between MYC-MAX and MNT-MAX interactions in B cells shifts in pre-malignant B cells towards a MYC driven transcriptional program. Moreover, we find that MAX loss leads to a significant reduction in MYC protein levels and downregulation of direct transcriptional targets, including regulators of MYC stability. This phenomenon is also observed in multiple cell lines treated with MYC-MAX dimerization inhibitors. Our work uncovers a layer of Myc autoregulation critical for lymphomagenesis yet partly dispensable for normal development.

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CUT&RUN comparing occupancy of MAX, MNT, MYC in MAX WT and KO B220+ cells

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CUT&RUN comparing the occupancy of MAX, MNT, MGA, MYC and RNA pol II Ser5 in a MAX null vs MAX reconstituted mouse SCLC line (mRPMaxKO)

Project description:The goal of this study was to compare the genomic occupancy of MAX, MNT, MGA and RNA pol II Ser5 in MAX restored versus MAX null SCLC (mRPMaxKO)

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Identification of MAX signature on MAX deficient SCLC cell lines

Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the transcription factor MAX.Human SCLC cell lines waere analyzed for mutations at the MAX locus. Those cell lines that were found mutated in MAX and showed no MAX protein expression were used as a models to restore the expression of MAX transcription factor, and Identify MAX signature on Human SCLC.

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Genomic occupancy of MAX and members of the MYC network in MAX WT and MAX null preSCs (polyclonal population)

Project description:Conventional crosslinked ChIP was performed on sgCtrl (control guide RNA) and sgMax (guide RNA against Max) transduced preSCs (early stage SCLC line). We find that loss of MAX leads to decreased MAX, MYC and MNT occupancy.

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Transcriptome profiles comparison between the B220+, CD27- and CD27+ NK cell subset

Project description:The cell lineage origin of interferon-producing killer dendritic cells (IKDC), which exhibit prominent anti-tumoral activity, has been subject to debate. Although IKDC were first described as a cell type exhibiting both pDC and NK cell properties, the current view reflects that IKDC merely represent activated NK cells expressing B220, which were thus renamed B220+ NK cells. Herein, we further investigate the lineage relationship of B220+ NK cells with regards to other NK cell subsets. We surprisingly find that, upon adoptive transfer, B220- NK cells did not acquire B220 expression, even in the presence of potent activating stimuli. These findings strongly argue against the concept that B220+ NK cells are activated NK cells in vivo. Moreover, we unequivocally demonstrate that B220+ NK cells are highly proliferative and differentiate into mature NK cells upon in vivo adoptive transfer. Additional phenotypic, functional and transcriptional characterizations further define B220+ NK cells as immediate precursors to mature NK cells. By analogy to pre-B cells and pre-DC, we propose that B220+ NK cells should be renamed pre-NK cells. The characterization of these novel attributes to pre-NK cells will guide the identification of their ortholog in humans, contributing to the design of potent cancer immunotherapies.

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