Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Next-Generation Sequencing Facilitates Quantitative Analysis of Wild Type, Mga-/-, L3mbtl2-/- and Pcgf6-/- Embryonic Stem Cells Transcriptomes

ABSTRACT: Purpose: The goals of this study are to compare Mga-/-, L3mbtl2-/-, Pcgf6-/- and Wild type embryonic stem cells transcriptome profiling (RNA-seq) and compare the target genes of Mga, L3mbtl2 and Pcgf6.

ORGANISM(S): Mus musculus

PROVIDER: GSE144141 | GEO | 2021/01/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

Project description:Max is an obligate dimerization partner for the Myc transcription factors and for several repressors, such as Mnt, Mxd1-4 and Mga, collectively thought to antagonize Myc function in transcription and oncogenesis. Mga, in particular, is part of the variant Polycomb group repressive complex PRC1.6. Here, we show that ablation of the distinct PRC1.6 subunit Pcgf6 – but not Mga – accelerates Myc-induced lymphomagenesis in Eµ-myc transgenic mice. Unexpectedly, however, Pcgf6 loss shows no significant impact on transcriptional profiles, in neither pre-tumoral B-cells, nor lymphomas. Altogether, these data unravel an unforeseen, Mga- and PRC1.6-independent tumor suppressor activity of Pcgf6.

2021-12-05 | GSE189999 | GEO

Pcgf6 suppresses Myc-induced lymphomagenesis [ChIP-seq]

2021-12-05 | GSE189989 | GEO

PRC1.6 molecule L3MBTL2 protects MYCN-amplified neuroblastoma cells via epigenetic gene suppression

Project description:Polycomb-group complexes are evolutionarily conserved epigenetic machineries that regulate stem cell fate decisions/development and are also implicated in tumorigenesis mainly by histone modification. PRC1 complexes mediates ubiquitylation of histone H2A on lysine 119 and consists of PRC1.1 to PRC1.6 complexes. Here, we studied the functional roles of a PRC1.6 molecule L3MBTL2 in neuroblastoma (NB) cells. L3MBTL2 knockout- and knockdown-experiments elucidated that L3MBTL2 depletion suppressed NB cell proliferation according with cell cycle arrest and gamma-H2A up-regulation. L3MBTL2 knockout profoundly suppressed xenograft tumor formation. Transcriptome analysis detected the suppressed cell cycle-related pathways and the activated the differentiation-related pathways. The remarkable de-repressed genes by the L3MBTL2 knockout were BRME1 and NRIP3. ChIP experiments showed co-localization of the PRC1.6 components PCGF6/E2F6/L3MBTL2 and MYCN at the transcription start sites (TSS) of these genes. L3MBTL2 knockout reduced H2AK119ub marks at the TSS regions but PCGF6 binding was heterogeneously changed. This study clarified the significance of PRC1.6 molecule L3MBTL2 in NB cell homeostasis and the epigenetic mechanism of the L3MBTL2-mediated gene suppression in NB that regulates the PRC1.6 complex localization and H2AK119 mono-ubiquitination in a gene locus-specific manner.

2023-09-26 | GSE201512 | GEO

RNA Sequencing Facilitates Quantitative Analysis of shL3MBTL2 ,CGA-OE and corresponding control Transcriptomes

Project description:L3MBTL2 is a crucial component of ncPRC1.6 and has been implicated in transcriptional repression and chromatin compaction. However, the repression mechanism of L3MBTL2 and its biological functions are largely undefined. CGA encodes the alpha subunit of glycoprotein hormones, however, we showed that CGA plays an individual tumor suppressor role in PDAC. The goals of this part study are to compare transcriptome profiling of PANC-1-shL3MBTL2 cells or PANC-1-CGA-OE cells to their corresponding control cells. By identifying differentially expressed genes (DEGs) and enrichment pathways, the mechanism of L3MBTL2 and CGA in pancreatic cancer can be better studied.

2022-01-01 | GSE184834 | GEO

PCGF6-PRC1 suppresses premature differentiation of embryonic stem cells by silencing germ cell-related genes [RNA-Seq]

Project description:Expression data of ES cells with or without Pcgf6, Ring1A/B, Max and Mga. Expression data of ES cells with or without Cbx1/3.

2017-03-16 | GSE84480 | GEO

SARS-CoV-2 Nsp6 damages Drosophila heart and mouse cardiomyocytes through MGA/MAX complex-mediated increased glycolysis

Project description:SARS-CoV-2 infection causes COVID-19, a severe acute respiratory disease associated with cardiovascular complications including long-term outcomes. The presence of virus in cardiac tissue of patients with COVID-19 suggests this is a direct, rather than secondary, effect of infection.Here, by expressing individual SARS-CoV-2 proteins in the Drosophila heart, we demonstrate interaction of virus Nsp6 with host proteins of the MGA/MAX complex (MGA, PCGF6 and TFDP1).

2022-10-04 | PXD036447 | Pride

L3MBTL2 protein acts in concert with PcG protein mediated monoubiquitination of H2A to establish a repressive chromatin structure [ChIP-Seq data].

Project description:Human MBT domain-containing protein L3MBTL2 was found to be an integral component of a protein complex that we termed Polycomb Repressive Complex 1-like 3 (PRC1L3) given the presence of the PcG proteins RING1, RING2 and PCGF6. L3MBTL2 binds chromatin in a histone modification-independent manner and is required for the repressive function of PRC1L3. PRC1L3 also contains E2F6 and CBX3, two factors with wellM-bM-^@M-^Pestablished functions in transcriptional repression. GenomeM-bM-^@M-^Pwide profiling identified several hundred genes that are simultaneously bound by L3MBTL2 and E2F6, preferentially around transcriptional start sites. Importantly, these genes are largely distinct from those targeted by other E2Fs or L3MBTL, another MBTM-bM-^@M-^Pdomain containing protein that interacts with RB1. H3K27 or H3K9 methylation, two chromatin modifications implicated in gene silencing, are not present on all L3MBTL2 target genes. L3MBTL2-specific RNAi results in altered target gene expression patterns and affects the differentiation program of hematopoietic cells. Our data suggest that repression of transcription via chromatin modulation, reflective of PRC1 function, can be achieved by multiple players and does not necessarily require the presence of histone lysine methylation marks. 7 total ChIP-seq datasets; one L3MBTL2 dataset done in duplicate in K562 cells; one E2F6 dataset done in duplicate in K562 cells; one H3K27me3 replicate dataset in K562 cells.

2011-06-07 | E-GEOD-28162 | biostudies-arrayexpress

L3MBTL2 in HEK293 cells - ChIPseq

Project description:To elucidate the (possibly sumo dependent) binding sites of L3MBTL2, wild type L3MBTL2, L3MBTL2-Flag and L3MBTL2-KR-Flag ChIPs from HEK293 cells were analyzed via ChIPseq

2014-01-14 | E-MTAB-1731 | biostudies-arrayexpress

L3MBTL2 protein acts in concert with PcG protein mediated monoubiquitination of H2A to establish a repressive chromatin structure [ChIP-Seq data].

Project description:Human MBT domain-containing protein L3MBTL2 was found to be an integral component of a protein complex that we termed Polycomb Repressive Complex 1-like 3 (PRC1L3) given the presence of the PcG proteins RING1, RING2 and PCGF6. L3MBTL2 binds chromatin in a histone modification-independent manner and is required for the repressive function of PRC1L3. PRC1L3 also contains E2F6 and CBX3, two factors with well‐established functions in transcriptional repression. Genome‐wide profiling identified several hundred genes that are simultaneously bound by L3MBTL2 and E2F6, preferentially around transcriptional start sites. Importantly, these genes are largely distinct from those targeted by other E2Fs or L3MBTL, another MBT‐domain containing protein that interacts with RB1. H3K27 or H3K9 methylation, two chromatin modifications implicated in gene silencing, are not present on all L3MBTL2 target genes. L3MBTL2-specific RNAi results in altered target gene expression patterns and affects the differentiation program of hematopoietic cells. Our data suggest that repression of transcription via chromatin modulation, reflective of PRC1 function, can be achieved by multiple players and does not necessarily require the presence of histone lysine methylation marks.

2011-06-07 | GSE28162 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data