Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

42 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of two mouse myc mutants Eilers-Mouse-MycKR6 vs Mycwt

ABSTRACT: Comparison gene regulation by two different Myc mutants

ORGANISM(S): Mus musculus

SUBMITTER: Nikita Popov

PROVIDER: E-MEXP-407 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

The ubiquitin ligase HectH9 regulates transcriptional activation by Myc and is essential for tumor cell proliferation.

Adhikary Sovana S Marinoni Federica F Hock Andreas A Hulleman Esther E Popov Nikita N Beier Rudi R Bernard Sandra S Quarto Micaela M Capra Maria M Goettig Stephan S Kogel Ulrike U Scheffner Martin M Helin Kristian K Eilers Martin M

Cell 20051101 3

The Myc oncoprotein forms a binary activating complex with its partner protein, Max, and a ternary repressive complex that, in addition to Max, contains the zinc finger protein Miz1. Here we show that the E3 ubiquitin ligase HectH9 ubiquitinates Myc in vivo and in vitro, forming a lysine 63-linked polyubiquitin chain. Miz1 inhibits this ubiquitination. HectH9-mediated ubiquitination of Myc is required for transactivation of multiple target genes, recruitment of the coactivator p300, and inductio ...[more]

PMID: 16269333

Similar Datasets

Transcription profiling of mouse splenic B cells expressing a dominant-negative p300 allele which lacks histone acetyltransferase activity

Project description:The p300 protein is one of more than 15 known mammalian HATs. We have used mice that carry a mutant allele of the p300 gene, which encodes a full-length protein that, however, lacks detectable acetyltransferase (AT)-activity and that acts in a dominant-negative manner. In addition, the allele is conditional, so that it can be expressed in a tissue-specific manner with the help of mice that express Cre-recombinase. Expression of the mutant allele specifically in B-cells, using CD19-cre mice, results in premature death with full penetrance from an autoimmune disease that closely mimics systemic lupus erythematosus (SLE) in its pathological manifestations.

2006-07-01 | E-MEXP-747 | biostudies-arrayexpress

RNAi knock down of HectH9 in human osteosarcoma samples to identify myc regulated genes

Project description:Analysis of Gene Regulation by Myc in the absence of HectH9

2005-10-17 | E-MEXP-406 | biostudies-arrayexpress

Transcription profiling of human carcinoma LS174T cells following depletion of Myc and Usp28 using shRNA

Project description:Analysis of gene expression following depletion of Myc and Usp28 using shRNA in colon carcinoma LS174T cells.

2007-04-19 | E-MEXP-1070 | biostudies-arrayexpress

Transcription profiling of blood vessel endothelial cells from wild type and PPARb knock-out mice

Project description:To elucidate the mechanisms underlying the perturbation of tumor vascularization in Pparb/ mice we performed matrigel plug assays23. Matrigel containing prostaglandin E2 (PGE2) and basic fibroblast growth factor (FGF-2) was injected subcutaneously into both wild-type and Pparb/ mice where it formed semi-solid plugs. These plugs became rapidly invaded by AQP-1 positive cells. To analyze differences between Pparb+/+ and Pparb/ samples we compare the gene expression profile of both samples by microarray analysis.

2007-12-01 | E-MEXP-983 | biostudies-arrayexpress

RNAi knock down of RET finger protein/ Tripartite protein in human osteosarcoma cell lines and analysis of Retinoblastoma protein dependent transcriptional changes

Project description:Analysis of Retinoblastoma protein (Rb) (Hs.408528) dependent transcriptional changes following siRNA mediated ablation of the RET finger protein/ Tripartite protein (RFP/TRIM27) (Hs.440382). Common reference design, two biological replicates with two technical replicates each.

2005-06-02 | E-MEXP-278 | biostudies-arrayexpress

Transcription profiling of human Soas-2 cells infected with adenoviruses expressing p53 proteins with charge-neutralizing or charge-inverting mutations in the H1 helix to investigate the role of the dimerization interface in p53 function

Project description:To investigate the role of the dimerization interface for p53 function, we introduced modest charge-neutralizing (R181→L "EL") and more severe charge-inverting (R181→E "EE" and E180→R, R181→E "RE") mutations into the H1 helix of the full-length p53 molecule. To characterize the nuclear transcriptional function of p53 mutants in an unbiased manner we employed gene expression profiling using cDNA microarrays. Saos-2 cells were infected with adenoviruses expressing the p53 proteins EE, EL, WT and RE which span the entire spectrum of apoptotic activity. Total cellular RNA was isolated 18 hours after infection when apoptosis had not yet occurred.

2010-04-01 | E-MEXP-1209 | biostudies-arrayexpress

Transcription profiling of human BJ fibroblasts after LIN-9 depletion by a shRNA

Project description:Aim: identification of differentially expressed genes after LIN-9 depletion.<br> <br> hTERT immortalized human BJ fibroblasts were infected with pMSCV-Blasticidin based retroviruses encoding a shRNA which targets human LIN-9 and the empty vector respectively.<br> After 4 days of selection total RNA was isolated. Cy3 and Cy5 labelled cDNA probes were generated using the CyScribe Post-labelling Kit (Amersham Biosiences).

2006-11-23 | E-MEXP-752 | biostudies-arrayexpress

Transcription profiling time series of mouse melanocytes transfected with an inducible version of the oncogenic receptor Xmrk, starved for 72 h and afterwards stimulated with EGF

Project description:Signaling pathways specifically induced by the oncogenic receptor Xmrk can be elucidated by comparing gene expression in cells with the activated receptor to gene expression in cells with the non-activated receptor. Mouse melanocytes transfected with an inducible version of the oncogenic receptor Xmrk, were starved for 72 h and afterwards stimulated with EGF. We compared cells stimulated for 15 minutes, 1 h, 2 h, 4 h, 8 h or 24 h, respectively, to unstimulated cells.

2008-08-31 | E-MEXP-1311 | biostudies-arrayexpress

Transcription profiling of mouseB-cell lymphomas with defined genetic alterations in p53 or p73

Project description:Induction of apoptosis by the tumor suppressor p53 is known to protect from Myc-driven lymphomagenesis. The p53 family member p73 is also a pro-apoptotic protein, which is activated in response to oncogenes like Myc. We therefore investigated whether p73 provides a similar protection from Myc-driven lymphomas as p53. To generate B-cell lymphomas with defined genetic alterations in p53 or p73, we crossed the Eµ-Myc transgenic to mice heterozygous for germ-line deletions in p53 (p53+/) or p73 (p73+/-). Lymphomas which have spontaneously developed in Eµ-Myc transgenic animals with the genotypes p53+/+, p53+/-, p73+/+, p73+/- or p73-/- were isolated when the animals were moribund and further processed for gene expression profiling with 22.5K cDNA microarrays.

2008-12-05 | E-MEXP-1620 | biostudies-arrayexpress

siRNAi knockdown of ZBTB4 in human SH-EP cells reveals Zbtb4 represses transcription of P21CIP1 and controls the cellular response to p53 activation

Project description:SH-EP cells were depleted for ZBTB4; Transfection of the cells were performed by oligofectamin RNAimax (Invitrogen) with siRNA smart pool (Dharmacon RNA Technologies); total RNA was isolated using RNAeasy Mini Kit (QIAGEN), preamplified, labeled with Cy3 and Cy5, respectively, and hybridized to cDNA-microarrays

2008-07-01 | E-MEXP-1554 | biostudies-arrayexpress

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