Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA expression profiling of livers from the conditional doxycyline-regulatable c-Myc-driven liver tumor mouse model during tumor development and regression.

ABSTRACT: Progressing and regressing liver tumor tissues (depending on the group) were subjected to miRNA profiling to identify the miRNA changes occuring during tumor development and regression. Conditional doxycyline-regulatable c-Myc-driven mice get liver tumors following doxycycline (Dox) withdrawal from their diet. When mice are re-administered Dox through their diet, tumors start to regress.

ORGANISM(S): Mus musculus Murid gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE152920 | GEO | 2021/08/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA expression profiling of livers from the conditional doxycyline-regulatable c-Myc-driven liver tumor mouse model during tumor development and regression.

Project description:MicroRNA expression profiling of livers from the conditional doxycyline-regulatable c-Myc-driven liver tumor mouse model during tumor development and regression.

| PRJNA640932 | ENA

Gene expression changes in response to doxycyline-induced expression of proinsulin (C96Y)-GFP in an INS-1 insulinoma cell line

Project description:A doxycyline-inducible INS-1 insulinoma cell line expressing proinsulin (C96Y)-GFP was engineered. Addition of doxycyline causes the production of the proinsulin (C96Y)-GFP, which is retained in the endoplasmic reticulum. This study analyzes the gene expression changes that occur after doxycyline-induced expression of proinsulin (C96Y)-GFP for 24h, 48h and 5 days. Expression changes were compared between control un-induced cells and cells treated with doxycyline. Three replicates (experiments) were performed for each time point.

2010-06-24 | GSE22537 | GEO

Gene expression changes in response to doxycyline-induced expression of proinsulin (C96Y)-GFP in an INS-1 insulinoma cell line

2010-07-29 | E-GEOD-22537 | biostudies-arrayexpress

MOT1-expression: Molecular mechanisms that distinguish TFIID housekeeping from regulatable SAGA promoters

Project description:An important distinction is frequently made between constitutively expressed housekeeping genes versus regulated genes. Although generally characterized by different DNA elements, chromatin architecture and cofactors, it is not known to what degree promoter classes strictly follow regulatability rules and which molecular mechanisms dictate such differences. We show that SAGA-dominated/TATA-box promoters are more responsive to changes in the amount of activator, even compared to TFIID/TATA-like promoters that depend on the same activator Hsf1. Regulatability is therefore an inherent property of promoter class. Further analyses show that SAGA/TATA-box promoters are more dynamic because TBP recruitment through SAGA is susceptible to removal by Mot1. In addition, the nucleosome configuration upon activator depletion shifts on SAGA/TATA-box promoters and seems less amenable to preinitiation complex formation. The results explain the fundamental difference between housekeeping and regulatable genes, revealing an additional facet of combinatorial control: an activator can elicit a different response dependent on core promoter class.

2016-11-11 | GSE81480 | GEO

HSF1-expression: Molecular mechanisms that distinguish TFIID housekeeping from regulatable SAGA promoters

2016-11-11 | GSE81479 | GEO

HSF1 ChIP-seq: Molecular mechanisms that distinguish TFIID housekeeping from regulatable SAGA promoters

2016-11-11 | GSE81787 | GEO

Hsf1-ChIP-on-chip: Molecular mechanisms that distinguish TFIID housekeeping from regulatable SAGA promoters

2016-11-11 | GSE81987 | GEO

An orthogonally regulatable DNA nanodevice for spatiotemporally controlled biorecognition and tumor treatment.

Project description: Not available

| S-EPMC7299621 | biostudies-literature

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

Reactivation of low avidity, tumor-specific CD8+ T cells correlates with immunotherapeutic efficacy of anti-PD-1

Project description:To investigate the phenotypic differences between high and low avidity tumor-specific CD8+ tumor-infiltrating lymphocytes (TILs) following anti-PD-1 therapy, we performed bulk RNA-seq on tetramer sorted GSW11-specific T cells from three regressing and three progressing CT26 tumors: giving three groups of total TethiCD8+CD44+ TILs from the progressing tumors (TetHighProg), TetloCD8+CD44+ TILs from the progressing tumors (TetLowProg) and TetloCD8+CD44+ TILs from the regressing tumors (TetLowReg), total 9 samples.

2023-08-23 | GSE221590 | 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