Unknown,Transcriptomics,Genomics,Proteomics

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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

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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]

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