In Stock Cell Lines
The Pdgfra Knockout C57BL/6 MSC Cell Line is a CRISPR/Cas9-edited murine mesenchymal stem cell line with disrupted platelet-derived growth factor receptor alpha (Pdgfra). Pdgfra encodes a receptor tyrosine kinase that transduces signals from PDGF ligands, activating PI3K/AKT and MAPK/ERK pathways to control proliferation, survival, and migration. This loss-of-function model enables detailed investigation of PDGFR??-dependent processes in MSC biology, fibrosis, and the tumor microenvironment. It is a reliable tool for Western blotting, migration assays, differentiation studies, and screening of PDGFR-targeted therapeutics.
CGN Knockout HT29 Polyclonal Cells
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LILRB4 Knockout HT29 Polyclonal Cells
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CLCN6 Knockout Hela Polyclonal Cells
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IFI27 Knockout CaSki Polyclonal Cells
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HCAR2 Knockout AGS Polyclonal Cells
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NFYA Knockout HEK293T Polyclonal Cells
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The Pdgfra Knockout C57BL/6 MSC Cell Line is a CRISPR/Cas9-edited knockout cell line designed to ablate expression of the platelet-derived growth factor receptor alpha (Pdgfra) gene in murine mesenchymal stem cells. This cell line provides a consistent, loss-of-function model for investigating PDGFR??-dependent signaling in stem cell biology, tissue repair, and pathological processes. The knockout was generated using CRISPR/Cas9-mediated gene disruption, eliminating functional PDGFR?? protein without exogenous tags or selection markers, preserving intrinsic MSC properties.
The host cell line is derived from the C57BL/6 inbred mouse strain, a widely used background in immunology and biomolecular research. C57BL/6 MSCs are multipotent stromal cells capable of differentiating into osteoblasts, chondrocytes, and adipocytes, and they exhibit robust immunomodulatory functions. These cells maintain stable diploid karyotypes and characteristic surface markers (e.g., Sca-1+, CD29+, CD44+, CD45?C, CD11b?C), ensuring reliability in extended culture and differentiation protocols.
Pdgfra encodes a single-pass receptor tyrosine kinase activated by PDGF ligands (PDGF-AA, PDGF-BB, PDGF-CC). Ligand binding induces autophosphorylation and recruitment of SH2 domain-containing adaptors Grb2, Shc, and the p85 regulatory subunit of PI3K. This initiates the RAS?CRAF?CMEK?CERK cascade, driving cell cycle progression through transcription factors such as c-Myc, c-Fos, and cyclin D1, and the PI3K?CAKT?CmTOR pathway, which promotes survival via Bcl-2 and regulates metabolic signaling. Additional intermediates include PLC??, and receptor crosstalk with integrins involves Rac and Cdc42 to control cytoskeletal dynamics. Upstream regulators like TGF-?? and IL-1?? modulate PDGFR?? activity under pathological conditions.
In MSCs, PDGFR?? is pivotal for self-renewal, migration, and lineage specification. Disruption of Pdgfra allows researchers to uncouple receptor-autonomous effects from compensatory pathways, revealing its role in osteogenic, adipogenic, and chondrogenic differentiation. Given its central position in fibrogenesis??acting downstream of TGF-?? to drive myofibroblast transdifferentiation??this knockout line is especially valuable for modeling pulmonary, hepatic, and renal fibrosis. It also serves as a tool for studying cancer-associated fibroblast biology, as PDGFR?? signaling is frequently hyperactivated in tumor stroma.
This knockout cell line supports numerous experimental applications. Standard characterization includes Western blotting for loss of PDGFR?? and reduced phospho-AKT (S473) and phospho-ERK (T202/Y204) following PDGF stimulation. Cellular assays with EdU or BrdU quantify proliferation defects, while transwell migration and osteogenic, adipogenic, and chondrogenic differentiation protocols assess functional consequences. RNA-seq profiling reveals PDGFR??-dependent gene networks. The line is suited for drug screening of PDGFR inhibitors, antifibrotic compound testing, and regenerative medicine studies. For more information, contact Ascent Research.
