In Stock Cell Lines
The Fgfr3 Knockout RCS Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the rat chondrosarcoma RCS line, providing a loss-of-function model for FGFR3, a receptor tyrosine kinase that negatively regulates chondrocyte proliferation. By eliminating FGFR3 expression, this model disrupts FGF-mediated signaling cascades. Downstream pathways normally activated by FGFR3 include MAPK/ERK and PI3K/AKT, mediated by adaptors such as FRS2 and GRB2. This cell line is ideal for studying skeletal dysplasia mechanisms, chondrosarcoma signaling, and FGF pathway biology using western blotting, RT-qPCR, and functional assays.
MAPK4 Knockout KYSE150 Polyclonal Cells
Cat. No. ARG12272
BUB1B Knockout HCT116 Polyclonal Cells
Cat. No. ARG23170
ABHD14B Knockout A2780 Polyclonal Cells
Cat. No. ARG28539
PEAK1 Knockout Hela Polyclonal Cells
Cat. No. ARG7841
MLKL Knockout HEK293T Polyclonal Cells
Cat. No. ARG3666
Rat Renal Artery Endothelial Cells
Cat. No. ARP0216
The Fgfr3 Knockout RCS Cell Line is a CRISPR/Cas9-edited knockout cell line generated from the rat chondrosarcoma RCS host line, designed to permanently disrupt the Fgfr3 gene. This engineered model eliminates functional FGFR3 protein expression, enabling precise dissection of FGFR3-mediated signaling in a chondrocyte context. The product is delivered as a validated cell line ready for downstream functional assays.
The parental RCS cell line is a well-established in vitro model of rat chondrosarcoma that retains key chondrocytic features, including the ability to synthesize cartilage extracellular matrix components. These cells express characteristic chondrocyte markers and respond to FGF stimulation, making them particularly suitable for investigating growth factor-driven cartilage biology and pathological processes affecting cartilage and bone.
FGFR3 encodes a receptor tyrosine kinase that is activated by FGF ligands such as FGF1, FGF2, and FGF9 in the presence of heparin sulfate proteoglycans. Ligand binding promotes receptor dimerization and autophosphorylation, which recruits intracellular adaptor proteins including FRS2, GRB2, SOS, SHC, and CBL. Downstream signaling propagates through multiple pathways: RAS-MAPK leading to ERK1/2 phosphorylation, PI3K-AKT, STAT cascades involving STAT1 and STAT3, and PLC??. In chondrocytes, FGFR3 predominantly functions as a negative regulator of proliferation, thereby controlling the tempo of endochondral bone formation.
Within the growth plate, FGFR3 signaling maintains proliferative quiescence of chondrocytes; its constitutive activation due to missense mutations results in skeletal dysplasias such as achondroplasia, hypochondroplasia, and thanatophoric dysplasia. Conversely, loss of FGFR3 activity can relieve proliferative restraints. In the RCS chondrosarcoma background, FGFR3 may also contribute to oncogenic signaling, as FGFR3 alterations are documented in bladder cancer and multiple myeloma. Knockout of Fgfr3 in this context disrupts these regulatory networks, offering a platform to examine both developmental and neoplastic roles of the receptor.
This cell line is well-suited for a variety of research applications. Western blot detection of phospho-FGFR3 and phospho-ERK1/2 provides direct readouts of pathway activity. RT-qPCR quantification of chondrogenic markers such as Col2a1 and Acan gauges differentiation status. Functional assays including proliferation, migration, and invasion studies help elucidate FGFR3??s contribution to chondrosarcoma behavior. The model also supports drug testing against FGFR3-dependent signaling and investigation of FGF pathway crosstalk. For additional details or to request a quotation, please contact Ascent Research.
