Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Truncated BRPF1 cooperates with Smoothened to induce adult Shh medulloblastoma

ABSTRACT: We performed ATAC-seq analysis, in order to understand the role of SmoM2 and truncated BRPF1 on the epigenetic landscape during medulloblastoma disruption

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE127733 | GEO | 2019/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Truncated BRPF1 cooperates with Smoothened to induce adult Shh medulloblastoma

Project description:Truncated BRPF1 cooperates with Smoothened to induce adult Shh medulloblastoma

| PRJNA525143 | ENA

Transcription profiling of mouse medulloblastoma

Project description:Dysregulatio of Hh signaling has been shown to be involved in the formation of human medulloblastoma. We generated a mouse model (CAGGS-CreER;R26-SmoM2) of Hh related tumors. We used microarray to profile gene expression in Hh induced mouse medulloblastoma and identified distinct classes of up-regulated or down-regulated genes during Hh dependent tumorigenesis . Experiment Overall Design: Medulloblastoma samples and adjacent wild type cerebellar tissue from CAGGS-CreER;R26-SmoM2 mice were isolated for RNA extraction and hybridization on Affymetrix microarrays.

2008-06-16 | E-GEOD-9299 | biostudies-arrayexpress

Sufu and Spop cooperate to suppress SHH medulloblastoma tumorigenesis via regulation of Gli2 protein stability [ChIP-seq]

Project description:GLI2 overexpression is a hallmark in SHH subgroup of medulloblastoma (SHH MB). Here we identify the targetome of Gli2 in two mouse models of SHH MB: SmoM2 overexpression and Sufu;Spop double knockout MB.

2018-12-13 | GSE112702 | GEO

Sufu and Spop cooperate to suppress SHH medulloblastoma tumorigenesis via regulation of Gli2 protein stability [RNA-seq]

Project description:GLI2 overexpression is a hallmark in SHH subgroup of medulloblastoma (SHH MB). Here we profile the transcriptome of two mouse models of SHH MB expressing high Gli2: SmoM2 overexpression and Sufu;Spop double knockout MB.

2018-12-13 | GSE112772 | GEO

Expression profiles of mouse medulloblastoma

2007-10-12 | GSE9299 | GEO

Genome sequencing of SHH medulloblastoma predicts genotype-related response to smoothened inhibition.

Project description: Not available

| S-EPMC4493053 | biostudies-literature

Developmental Basis of SHH Medulloblastoma Heterogeneity

Project description:Single-Nucleus RNA-Sequencing and Single-Cell RNA-Sequencing from SHH Medulloblastoma Tumors with MBEN histology

2023-11-21 | GSE214469 | GEO

SHH medulloblastoma samples

Project description:Sequencing data of human SHH medulloblastoma samples

| EGAS00001000607 | EGA

Expression data of endothelial cells from mouse hindbrain and genetic Wnt-medulloblastoma and Shh-medulloblastoma mouse models

Project description:The childhood brain tumour medulloblastoma includes four subtypes with very different prognoses. Here, we show that paracrine signals driven by mutant Beta-Catenin in WNT-medulloblastoma â an essentially curable form of the disease â induce an aberrant fenestrated vasculature that permits the accumulation of high levels of intra-tumoural chemotherapy and a robust therapeutic response. In contrast, SHH-medulloblastoma â a less curable disease subtype â contains an intact blood brain barrier, rendering this tumour impermeable and resistant to chemotherapy. Remarkably, the medulloblastoma-endothelial cell paracrine axis can be manipulated in vivo, altering chemotherapy permeability and clinical response. Thus, medulloblastoma genotype dictates tumour vessel phenotype, explaining in part the disparate prognoses among medulloblastoma subtypes and suggesting an approach to enhance the chemoresponsiveness of other brain tumours. We used microarrays to detail the global program of gene expression within endothelial cells from normal mouse hindbrain and genetic mouse models of different medulloblastoma subtypes to identify and verify up-regulated and down-regulated genes Endothelial cells were isolated from adult mouse hindbrain and genetic mouse models of Wnt and Shh-medulloblastoma using Cd-144 and Cd-105 antibodies based magnetic sorting. RNA was extracted and used for hybridization on Affymetrix microarrays. We sought to identify changes in endothelial gene expression patterns based on the surrounding microenvironment, so we purified endothelial cells from normal mouse brain or tumors from genetic mouse models. These include the Shh-medulloblastoma model (Ptch+/-; Ink4c -/-) and Wnt-medulloblastoma model (Blbp-Cre; mutant Ctnnb1+/-; p53-/-; mutant Pik3ca +/-)

2016-04-05 | E-GEOD-73753 | biostudies-arrayexpress

Gene expression profiling of constitutive activation of Smoothened in the mouse uterus

Project description:In order to gain a better understanding of Ihh action during embryo implantation, we constitutively activated Smo in the murine uterus using the PRcre mouse model (PRcre/+SmoM2+; SmoM2). Female SmoM2 mice were infertile. They exhibited normal serum progesterone levels and normal ovulation, but ova failed to be fertilized in vivo and the uterus failed to undergo the artificially induced decidual response. SmoM2 mice exhibited uterine hypertrophy. The endometrium had a reduced number of uterine glands and the endometrial stroma lost its normal morphologic characteristics. Microarray analysis of 3 month old SmoM2 uteri demonstrated a chondrocytic signature and confirmed that constitutive activation of SmoM2 increased extracellular matrix production. Thus, constitutive activation of Smo in the mouse uterus alters the extracellular matrix which interferes with early pregnancy. Keywords: two group comparison We constitutively activated Hh signaling in the uterus by the expression of a mutant SmoM2 allele. We crossed these mice to the PRcre mouse model to constitutively activate Smo in the murine uterus (PRcre/+SmoM2+; SmoM2). High density DNA microarray analysis was performed on 3 month old control and SmoM2 uteri.

2010-04-13 | E-GEOD-17263 | biostudies-arrayexpress

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