Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of rat FGFR3-K650E mutant and wild type PC12 cells

ABSTRACT: To investigate signaling pathways activated by FGFR3 mutations through an analysis of altered expression of downstream transcriptional targets, we performed gene expression profiling of stably transfected inducible PC12 cells expressing a chimeric receptor (PFR3) consisting of the extracellular domain of human platelet derived growth factor receptor (PDGFR) and the transmembrane and intracellular domains of human FGFR3 under the control of the zinc inducible metalliothionein promoter. Cells expressing the wildtype receptor (i.e. zinc induced) were compared to cells expressing the mutant receptor PFR3K650E, which contains the thanatophoric dysplasia type II mutation, K650E. See PubMed ID for further description of samples.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Barbara Apostol

PROVIDER: E-GEOD-2606 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Sustained ERK1/2 but not STAT1 or 3 activation is required for thanatophoric dysplasia phenotypes in PC12 cells.

Nowroozi Nakisa N Raffioni Simona S Wang Tracy T Apostol Barbara L BL Bradshaw Ralph A RA Thompson Leslie Michels LM

Human molecular genetics 20050420 11

Mutations in fibroblast growth factor receptor 3 (FGFR3) cause the most common genetic form of short-limbed dwarfism, achondroplasia (ACH), as well as neonatal lethal forms, thanatophoric dysplasia (TD) I and II. The causative mutations induce graded levels of constitutive activation of the receptor that correspond to the severity of the disorder, resulting in premature entry into hypertrophic differentiation and reduced proliferation of chondrocytes in developing cartilage. Although FGFR3 promo ...[more]

PMID: 15843401

Similar Datasets

Gene expressing profiling of PC12 cells expressing the FGFR3 mutation responsible for thanatophoric dysplasia type II

Project description:To investigate signaling pathways activated by FGFR3 mutations through an analysis of altered expression of downstream transcriptional targets, we performed gene expression profiling of stably transfected inducible PC12 cells expressing a chimeric receptor (PFR3) consisting of the extracellular domain of human platelet derived growth factor receptor (PDGFR) and the transmembrane and intracellular domains of human FGFR3 under the control of the zinc inducible metalliothionein promoter. Cells expressing the wildtype receptor (i.e. zinc induced) were compared to cells expressing the mutant receptor PFR3K650E, which contains the thanatophoric dysplasia type II mutation, K650E. See PubMed ID for further description of samples. Keywords = thanatophoric dysplasia Keywords = FGFR3 Keywords = PC12 Keywords = ERK1/2 Keywords: repeat sample

2005-05-06 | GSE2606 | GEO

Microarray of Human astrocytes transduced with lentivirus expressing FGFR3-TACC3 treated with vehicle, FGFR3-TACC3 treated with the FGFR inhibitor PD173074 for 12h, FGFR3-TACC3-K508M treated with vehicle or empty vector treated with vehicle

Project description:In order to interrogate the transcriptional changes elicited by FGFR3-TACC3, we expressed the FGFR3-TACC3 fusion protein in human astrocytes and compared the global gene expression profiles of cells treated with a specific inhibitor of FGFR3-TK (PD173074) or vehicle. FGFR3-TACC3 expressing HA were also compared with HA that expressed the kinase-inactive FGFR3-TACC3 (FGFR3-TACC3-K508M) and HA transduced with the empty vector. Gene Ontology-guided enrichment map demonstrated that, besides the expected enrichment for mitotic activity, oxidative phosphorylation and mitochondrial biogenesis were the most significant biological functions enriched in HA expressing active FGFR3-TACC3.

2017-10-17 | E-MTAB-6037 | biostudies-arrayexpress

FGFR3-shRNA induced transcriptional changes in RT112 bladder cancer cells

Project description:Aberrant activation of FGFR3 via overexpression or mutation is a frequent feature of bladder cancer; however, its molecular and cellular consequences and functional relevance to carcinogenesis are not well understood. In this study with a bladder carcinoma cell line expressing inducible FGFR3 shRNAs, we sought to identiy transcriptional targets of FGFR3 and investigate their contribution to bladder cancer development. Bladder cancer cell line RT112 was transduced with a doxycycline-inducible control EGFP shRNA or three independent FGFR3 shRNAs, designated FGFR3 shRNA 2-4, FGFR3 shRNA 4-1 and FGFR3 shRNA 6-16. These four cell lines were treated with or without doxycycline for 48 hr to deplete FGFR3 protein prior to the isolation of mRNA for microarray analysis. Genes that were differentially expressed after doxycycline induction in all three FGFR3-depleted cell lines but not in the control cell line were considered potential FGFR3-regulated genes. Each treatment group was run in triplcates, and there are 24 samples.

2012-11-07 | E-GEOD-41035 | biostudies-arrayexpress

FGFR3-shRNA induced transcriptional changes in RT112 bladder cancer cells

2012-11-07 | GSE41035 | GEO

RNAseq and scRNAseq analysis of UPFL mouse tumors

Project description:Fibroblast growth factor receptor 3 (FGFR3) is altered in up to 50% of urothelial cancers (UC), yet its functional impact is not fully understood. We generated a Cre-inducible FGFR3 S249C allele (LSL-FGFR3 S249C) to understand the functional impact of FGFR3 activation on UC biology, the immune microenvironment, and how FGFR inhibition combines with PD1 immune checkpoint inhibition (ICI). Uroplakin3a (Upk3a) driven expression of Trp53 R270H and FGFR3 S249C (UPFL) promoted tumor formation.

2024-01-01 | GSE217093 | GEO

A Study of [225Ac]-FPI-1966 in Participants With Advanced Solid Tumours

Project description:This first-in-human study evaluates safety, tolerability and distribution of [225Ac] FPI-1966, [111In]-FPI-1967, and vofatamab in patients with FGFR3-expressing solid tumors.

| 2726960 | ecrin-mdr-crc

FOXO3a and beta-catenin transcriptional profile in human colon cancer cell line DLD1

Project description:We established a model system in human DLD1 colon cancer cells to study the transcriptional crosstalk between FOXO3A and beta-Catenin. Thereby, translocation to the nucleus of a AKT-insensitive mutant (T32A, S253A, S315A) of human FOXO3A fused to the ligand binding domain of human estrogen receptor can be induced by exposure to 4-hydroxy-tamoxifen. Furthermore, expression of a stable mutant (S33Y) of human beta-catenin is doxycycline inducible. Addition of those drugs separately or in combination allows identification of common or excusive target gene sets.

2012-05-01 | E-MEXP-3262 | biostudies-arrayexpress

Expression data from inducible ES stable cell lines

Project description:In order to identify the effects of the induction of the gene of interest on the mouse ES transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the different inducible cell lines Transcriptome analysis of the inducible transgenic mouse ES cell lines For the analysis on the different inducible cell lines, total RNA was extracted from three biological replicates grown in medium deprived of Tetracycline for 17 and 24 hours; RNA extracted from un-induced clones was used as control. Total RNA extracted from parental cell line EBRTcH3 (EB3) was used as additional control.

2012-12-03 | E-GEOD-32015 | biostudies-arrayexpress

Ikaros responsive genes in the T29 cell line

Project description:The mouse Ikaros-deficient thymic lymphoma cell line T29 was transduced with an empty retrovirus (MigR1) or a retrovirus expressing an fusion proein between Ikaros1 and the ligand binding domain of the estrogen receptor. Cells trreated with ethanol or 4-hydroxy-tamoxyfen (4OHT) for 24h were profiled. We used expression of an inducible ersion of the Ikaros protein in an Ikaros-deficient cell line to identify Ikaros-regulated genes

2013-04-17 | E-GEOD-46088 | biostudies-arrayexpress

Notch responsive genes in the T29 cell line

Project description:The mouse Ikaros-deficient thymic lymphoma cell line T29 was transduced with a retrovirus expressing an fusion protein between a dominant-negative form of Mastermind and the ligand binding domain of the estrogen receptor. Cells trreated with Ethanol or 4-hydroxy-tamoxyfen for 24h were profiled. We used expression of an inducible ersion of the dominant negative Mastermind protein in an Ikaros-deficient cell line to identify Notch-regulated genes

2013-04-17 | E-GEOD-46089 | 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