Transcriptome profile of RCS chondrocyte wt cell line and RCS chondrocyte obtained from a clone ko for the FGF receptors FGFR3 and FGFR4
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA493251 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7905500.fastq.gz | Fastqsanger.gz | |||
| SRR7905501.fastq.gz | Fastqsanger.gz | |||
| SRR7905492.fastq.gz | Fastqsanger.gz | |||
| SRR7905502.fastq.gz | Fastqsanger.gz | |||
| SRR7905493.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:To understand the transcriptomic effect of FGF18 treatment on Chondrocytes cells from wt rat and on Chondrocytes obtained from a clone ko for the FGF receptors FGFR3 and FGFR4, we performed Quant-seq experiments. Both cell lines were treated with Fibroblast growth factor 18 (FGF18), while untreated cells were used as control.
2020-07-13 | GSE120516 | GEO
Project description:Gene expression profiling of newborn lung tissue revealed few changes in compound FGFR3/FGFR4 deficient mice, consistent with their normal lung morphology at birth, suggesting the sequence of events leading to the phenotype initiates after birth in this model. Profiling of 4 week-old lung tissues revealed an induction of genes related to elastic fiber assembly in compound mutants. Lung RNA isolated from three animals of each genotype-age group were pooled for each Affymetrix chip (n=3 chips for each, except n=2 for wild type at 4 weeks.
2010-04-12 | E-GEOD-15452 | biostudies-arrayexpress
Project description:Gene expression profiling of newborn lung tissue revealed few changes in compound FGFR3/FGFR4 deficient mice, consistent with their normal lung morphology at birth, suggesting the sequence of events leading to the phenotype initiates after birth in this model. Profiling of 4 week-old lung tissues revealed an induction of genes related to elastic fiber assembly in compound mutants.
2010-03-31 | GSE15452 | GEO
Project description:To understand the determinants of chondrocyte FGF inhibitory response we sought to identify the unique set of proteins whose phosphorylation status is changed upon FGF treatment. RCS (Rat ChondroSarcoma) (RCS) cells were used for our experiments as a well-accepted model of proliferative chondrocytes which respond to FGF signaling with growth arrest Chondrocytes were treated with FGF1 and, as a control, cell cycle changes were monitored by FACScan analysis to demonstrate strong (around 95%) downregulation of S-phase at 24h. Three independent experiments were performed to obtain statistically representative datasets. We quantified 8299 proteins were quantified in the global proteome analysis using only unique or and razor peptides for quantitation . All proteins were identified in at least two replicates of a single treatment set by 2 or more peptides with 1% FDR Inclusion requirements for a single proteins were 1) two or more peptides identified with 51% FDR and 2) peptides that proteins were identified in at least 2 replicates of a single sample set.
| MSV000080259 | MassIVE
Project description:Achondroplasia (ACH), the most common form of human dwarfism is caused by a mutation in the Fibroblast Growth Factor Receptor 3 (FGFR3) gene, resulting in constitutive activation of the receptor. In order to gain insight into molecular mechanisms involved in the physiopathology, a conditional mouse model carrying the Y367C mutation corresponding to the human Y373C TDI mutation was produced (fgfr3neoY367C/+). Crossing these mice with CMV-CRE mice produces dwarf fgfr3Y367C/+ and fgfr3+/+ controls littermates. Dwarf fgfr3Y367C/+ mice exhibited skeletal dysplasia at birth, the phenotype becoming progressively more pronounced as the mice got older, with reduced length of long bone, narrow trunk, short ribs and macrocephaly. Histological examination of epiphyseal growth plates showed a disorganized growth plate, with reduced size of the hypertrophic and proliferative zone and an accelerated secondary ossification center formation (full phenotype description in Pannier S et al, Activating Fgfr3 Y367C mutation causes hearing loss and inner ear defect in a mouse model of chondrodysplasia. Biochimica et biophysica acta 2009; Pannier S et al, Delayed bone age due to a dual effect of FGFR3 mutation in Achondroplasia. Bone 2010; Jonquoy A et al, A novel tyrosine kinase inhibitor restores chondrocyte differentiation and promotes bone growth in a gain-of-function Fgfr3 mouse model. Human molecular genetics 2012; Martin L et al, Constitutively-active FGFR3 disrupts primary cilium length and IFT20 trafficking in various chondrocyte models of achondroplasia. Human molecular genetics 2018).
2020-12-31 | GSE145821 | GEO
Project description:The mannose-6-phosphate (M6P) pathway is critical for lysosome biogenesis, facilitating the trafficking of hydrolases to lysosomes to ensure cellular degradative capacity [1], [2]. Fibroblast Growth Factor (FGF) signaling, a key regulator of skeletogenesis [3], has been linked to the autophagy-lysosomal pathway in chondrocytes [4], [5], [6], but its role in lysosome biogenesis remains poorly characterized. Here, using mass spectrometry, lysosome immune-purification, and functional assays, we reveal that chondrocytes lacking FGF receptors 3 and 4 exhibit dysregulations of the M6P pathway, resulting in hypersecretion of lysosomal enzymes and impaired lysosomal function. We found that FGF receptors control the expression of M6P receptors genes in response to FGF stimulation and during cell cycle via TFEB/TFE3 activation. Notably, restoring MPRs function—either through gene expression or activation of TFEB—rescues lysosomal defects in FGFR3;4-deficient chondrocytes. These findings uncover a novel mechanism by which FGF signaling regulates lysosomal function, offering insights into the control of chondrocyte catabolism and the understanding of FGF-related human diseases.
2025-08-25 | PXD063031 | Pride
Project description:The mannose-6-phosphate (M6P) pathway is critical for lysosome biogenesis, facilitating the trafficking of hydrolases to lysosomes to ensure cellular degradative capacity [1], [2]. Fibroblast Growth Factor (FGF) signaling, a key regulator of skeletogenesis [3], has been linked to the autophagy-lysosomal pathway in chondrocytes [4], [5], [6], but its role in lysosome biogenesis remains poorly characterized. Here, using mass spectrometry, lysosome immune-purification, and functional assays, we reveal that chondrocytes lacking FGF receptors 3 and 4 exhibit dysregulations of the M6P pathway, resulting in hypersecretion of lysosomal enzymes and impaired lysosomal function. We found that FGF receptors control the expression of M6P receptors genes in response to FGF stimulation and during cell cycle via TFEB/TFE3 activation. Notably, restoring MPRs function—either through gene expression or activation of TFEB—rescues lysosomal defects in FGFR3;4-deficient chondrocytes. These findings uncover a novel mechanism by which FGF signaling regulates lysosomal function, offering insights into the control of chondrocyte catabolism and the understanding of FGF-related human diseases.
2025-08-25 | PXD063029 | Pride
Project description:The mannose-6-phosphate (M6P) pathway is critical for lysosome biogenesis, facilitating the trafficking of hydrolases to lysosomes to ensure cellular degradative capacity [1], [2]. Fibroblast Growth Factor (FGF) signaling, a key regulator of skeletogenesis [3], has been linked to the autophagy-lysosomal pathway in chondrocytes [4], [5], [6], but its role in lysosome biogenesis remains poorly characterized. Here, using mass spectrometry, lysosome immune-purification, and functional assays, we reveal that chondrocytes lacking FGF receptors 3 and 4 exhibit dysregulations of the M6P pathway, resulting in hypersecretion of lysosomal enzymes and impaired lysosomal function. We found that FGF receptors control the expression of M6P receptors genes in response to FGF stimulation and during cell cycle via TFEB/TFE3 activation. Notably, restoring MPRs function—either through gene expression or activation of TFEB—rescues lysosomal defects in FGFR3;4-deficient chondrocytes. These findings uncover a novel mechanism by which FGF signaling regulates lysosomal function, offering insights into the control of chondrocyte catabolism and the understanding of FGF-related human diseases.
2025-08-25 | PXD063036 | Pride
Project description:To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of UMUC-14 cell lines, which endogenously expressed a mutated activated form of FGFR3 (FGFR3-S249C), the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.
2020-12-31 | GSE125547 | GEO