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

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

PROVIDER: PRJNA610284 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11237724_1.fastq.gz	Fastqsanger.gz
	SRR11237724_2.fastq.gz	Fastqsanger.gz
	SRR11237725_1.fastq.gz	Fastqsanger.gz
	SRR11237725_2.fastq.gz	Fastqsanger.gz
	SRR11237726_1.fastq.gz	Fastqsanger.gz

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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.

2020-06-06 | GSE146385 | GEO

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)

2020-06-06 | GSE146388 | GEO

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.

2019-06-20 | GSE132967 | GEO

MAX-mutant small cell lung cancers sustain impaired activities of the MGA-dependent ncPRC1

Project description:The MYC-axis is disrupted in cancer, mostly by activation of the MYC-oncogenes but also through inactivation of the MYC-partner, MAX, or of the MAX-partner, MGA, both also members of the polycomb repressive complex, ncPRC1.6. Here, we use genetically modified MAX-deficient small cell lung cancer (SCLC) cells and apply genome wide and proteomics analysis to study the tumor suppressor function of MAX. We find that MAX-mutant SCLCs classify as ASCL1-type and lack MYC-transcriptional activities. MAX-restitution triggers pro-differentiation expression profiles that shift when MAX and oncogenic MYC (HMYC/MAX) are co-expressed. Despite the ncPRC1.6 can be formed, the lack of MAX restricts global MGA-occupancy, selectively driving its recruitment towards E2F6-motifs. Conversely, MAX-restitution enhances MGA-occupancy and global gene repression of genes involved in different functionalities, including stem-cell and DNA repair/replication. Collectively, these findings reveal that MAX-mutant SCLCs have ASCL1-characteristics, are MYC-independent and their oncogenic features include a deficient ncPRC1.6-mediated gene repression.

2021-01-18 | GSE144457 | GEO

CUT&RUN studies comparing occupancy of MAX, MGA, MYC and L3MBTL2 occupancy in Empty vector and sgMGA transduced A549 lung adenocarcinoma cells

Project description:The goal of this study was to examine the genomic occupancy of MAX, MGA, MYC and L3MBTL2 in MGA depleted vs. control cells

2020-11-16 | GSE161539 | GEO

MAX-mutant small cell lung cancers exhibit impaired activities of MGA-dependent ncPRC1.6.

Project description:The MYC axis is commonly disrupted in cancer, mostly by activation of the MYC family of oncogenes, but also by genetic inactivation of MAX, the obligate partner of MYC, and of the MAX partner, MGA, both of which are members of the polycomb repressive complex, ncPRC1.6. While the oncogenic properties of the MYC family have been extensively studied, the tumor suppressor functions of MAX and MGA and the role of the MYC genes in MAX-mutant cells remain unclear. To address these knowledge gaps, we used chromatin immunoprecipitation, RNA-sequencing and mass spectrometry-based proteomic analysis in MAX-restituted and MYC oncogenic-transformed cell lines derived from human small cell lung cancer (SCLC), which is a high-grade neuroendocrine type of lung cancer. We found that MAX-mutant SCLC cells express ASCL1 and ASCL1-dependent targets, implying that these cells belong to the ASCL1-dependent group of SCLCs. In the absence of MAX, even after ectopic overexpression of MYC, we found no recruitment of MYC to the DNA. Furthermore, MAX reconstitution triggered pro-differentiation expression profiles that shifted when MAX and oncogenic MYC were co-expressed. Although ncPRC1.6 could be formed, the lack of MAX restricted global MGA occupancy, selectively driving its recruitment towards E2F6 motifs. Conversely, MAX restitution enhanced MGA occupancy and global gene repression of genes involved in different functions, including stem-cell and DNA repair/replication. Our data reveal that MAX-mutant SCLCs have ASCL1 characteristics, and are MYC-independent, and that their oncogenic features include deficient ncPRC1.6-mediated gene repression.

2021-09-22 | PXD017658 | Pride

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: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)

| PRJNA610291 | ENA

Sirt1, p53 and p38MAPK are crucial regulators of detrimental phenotypes of ESCs with Max expression ablation

Project description:Ablation of expression of the Max gene encoding a Myc protein partner in ES cells provoked two major phenomena, i.e. loss of pluripotency and apoptotic cell death. We found that nicotinamide (Nam) significantly alleviates these Max expression ablation-coupled phenotypes in ES cells. To see the alleviation effect of Nam on the overall expression profile of Max-null ES cells whose Max expression is controlled by the tet-off system, we eliminated Max expression by adding doxycycline (Dox) in the presence of Nam.

2012-08-28 | GSE37917 | GEO

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.

2013-12-28 | GSE48559 | GEO

Sequence specificity incompletely defines the genome-wide occupancy of Myc

Project description:The Myc-Max heterodimer is a DNA binding protein that regulates expression of a large number of genes. Genome occupancy of Myc-Max is thought to be driven by E-boxes (CACGTG or variants) to which the heterodimer binds in vitro. By analyzing ChIP-Seq datasets, we demonstrated that the positions occupied by Myc-Max across the human genome correlate with the RNA polymerase II (Pol II) transcription machinery better than with E-boxes. Metagene analyses showed that in promoter regions, Myc was uniformly positioned about 100 bp upstream of essentially all promoter proximal paused polymerases with Max about 10 bp upstream of Myc. We re-evaluated the DNA binding properties of full length Myc-Max proteins using electrophoretic mobility shift assays (EMSA) and protein-binding microarrays (PBM). EMSA results demonstrated Myc-Max heterodimers have high affinity for both E-box containing and non-specific DNA. Quantification of the relative affinities of Myc-Max for all possible 8- mers using PBM assays showed that sequences surrounding core 6-mers significantly affect binding. Comparing to the in vitro sequence preferences, Myc-Max genomic occupancy measured by ChIP-Seq was largely, although not completely, independent of sequence specificity. Our results suggest that the transcription machinery and associated promoter accessibility play an important role in genomic occupancy of Myc.

2014-09-22 | GSE58570 | GEO

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