Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Max as a biological blockade that restricts meiotic process in ESCs

ABSTRACT: We explored Max ablation-mediated up-regulation of germ-related genes, especially meiosis-related genes in mouse embryonic stem cells which were cultured either under conventional mouse ES medium or 2i condition using inhibitors against MEK and GSK3b.

ORGANISM(S): Mus musculus

PROVIDER: GSE65700 | GEO | 2016/03/31

SECONDARY ACCESSION(S): PRJNA274741

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Max as a biological blockade that restricts meiotic process in ESCs

Project description:We explored Max ablation-mediated up-regulation of germ-related genes, especially meiosis-related genes in mouse embryonic stem cells which were cultured either under conventional mouse ES medium or 2i condition using inhibitors against MEK and GSK3b. Effect of culture conditions (conventional mouse ES medium or 2i condition) on the expression profile of germ-related genes in Max expression ablated ES cells were examined using inducible Max-null ES cells in which Max gene had been homozygously disrupted, but carries Max cDNA in ROSA26 locus with tetracycline-off system.

2016-03-31 | E-GEOD-65700 | biostudies-arrayexpress

Derivation of ground-state female ESCs maintaining gamete-derived DNA methylation

Project description:Inhibitors of MEK1/2 and Gsk3b, known as '2i' culture conditions, enhance the derivation of embryonic stem cells (ESCs) and promote ground-state pluripotency in rodents 1,2. Here we show that the derivation of female mouse ESCs in the presence of 2i (2i-ESCs) results in a widespread loss of DNA methylation including a massive erasure of genomic imprints. Despite this global loss of DNA methylation, the early-passage 2i-ESCs efficiently differentiate into somatic cells and this process requires genome-wide de novo DNA methylation. However, the majority of imprinting control regions (ICRs) remain unmethylated in the 2i-ESC-derived differentiated cells. Consistently, 2i-ESCs exhibit impairment of autonomous embryonic and placental development by tetraploid embryo complementation and nuclear transplantation. We identified the derivation conditions of female ESCs that display 2i-ESC-like transcriptional signatures while preserving gamete-derived DNA methylation and autonomous developmental potential. Upon prolonged culture, however, female ESCs exhibit ICR demethylation, regardless of culture conditions. Our results provide insights into derivation of female ESCs reminiscent of ICM of preimplantation embryos. S-ESCs are ESCs established under serum-containing medium. 2i_S_ESCs are ESCs established in 2i-containing medium, followed by maintenance in serum-containing medium.

2017-07-27 | GSE84164 | GEO

Effect of ablation of Max gene expression on ES cells cultured under conventional or 2i/Nam condition.

Project description:c-Myc is one of key players that are crucially involved in maintaining the undifferentiated state and the self-renewal of ESCs. To understand the mechanism by which c-Myc helps preserve these prominent characteristics of ESCs, we generated null-ES cells for the Max gene, which encodes the best characterized partner protein for all Myc family proteins. Although Myc/Max complexes have been widely regarded as crucial regulators of the ESC status, our data reveal that ESCs do not absolutely require these complexes in so-called ground state or related conditons and that this requirement is restricted to conventional ES culture conditions without using a MAPK inhibitor. Simply Dox-treated or Nanog (WT or D67G mutant)-rescued Max-null ESCs which were cultured under conventional culture condition and 2i/Nam-treated completely Max-null ES cells from which Dox-regulatable cDNA was removed were used for RNA source. Samples from Dox-untreated Max-null ESCs cultured under conventional culture condition were used as reference samples for Dox-treated cells and Nanog-rescued cells, while a sample from wild-type ESCs cultured under 2i/Nam condition was used as a reference sample for completely Max-null ES cells cultured with 2i/Nam.

2011-07-19 | E-GEOD-27881 | biostudies-arrayexpress

Ablation of Max expression induces meiotic onset in sexually undifferentiated germ cells

Project description:MAX (MYC Associated Factor X) is generally known as a mandatory partner for MYC transcription factor, which activates various genes involved in cell growth and metabolism. On the other hand, MAX, when interacting with MGA, forms the polycomb repressive complex (PRC) 1.6, one of the subtypes of PRC1, which directs the transcriptionally repressed chromatin state. Although physiological significance is not known at present, we have previously demonstrated that mouse embryonic stem cells (ESCs) bear a potential to onset meiosis, albeit not germ cells, and PRC1.6 prevent ESCs from their ectopic onset of meiosis (Suzuki et al., 2016, Nat. Commun. 7:11056 doi: 10.1038/ncomms11056). In this study, we aimed to investigate the role of Max in germ cells in vivo by performing the primordial germ cell-specific knockout of the Max gene.

2024-03-13 | GSE233556 | GEO

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

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

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

2012-08-28 | E-GEOD-37917 | biostudies-arrayexpress

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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