In Stock Cell Lines
Mus musculus (Mouse)
Skin
Adherent
The Egfr Knockout B16 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring targeted disruption of the Egfr gene in the B16 murine melanoma background. This line eliminates EGFR, a receptor tyrosine kinase that, upon ligand binding, activates key pathways such as the GRB2-mediated MAPK/ERK and PI3K-AKT cascades, driving proliferation and survival. This knockout model enables rigorous investigation of EGFR-dependent mechanisms in melanoma progression, metastasis, and therapeutic resistance. It is ideal for in vitro assays, drug screening, and syngeneic mouse models for immunotherapy studies.
DDAH2 Knockout Raji Polyclonal Cells
Cat. No. ARG0912
MAPK4 Knockout TE1 Polyclonal Cells
Cat. No. ARG12177
ENG Knockout Hela Polyclonal Cells
Cat. No. ARG9036
ASIC1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG34636
KIF2A Knockout A549 Polyclonal Cells
Cat. No. ARG34480
MS4A1 Knockout Raji Polyclonal Cells
Cat. No. ARG1275
The Egfr Knockout B16 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the B16 murine melanoma cell line, with targeted disruption of the Egfr gene. This ablation eliminates epidermal growth factor receptor (EGFR) expression, providing a defined loss-of-function model for investigating EGFR-dependent signaling in a melanocytic tumor context. The cell line is suitable for both in vitro experiments and in vivo syngeneic tumor studies.
The parental B16 cell line originates from a C57BL/6 mouse melanoma and represents a highly aggressive, pigmented melanocytic tumor model. B16 cells exhibit robust proliferation and metastasis in syngeneic, immunocompetent C57BL/6 hosts, enabling comprehensive analysis of tumor progression, immune evasion, and therapeutic responses within an intact immune microenvironment.
EGFR is a receptor tyrosine kinase activated by EGF family ligands such as EGF and TGF-??. Ligand binding induces dimerization and autophosphorylation, recruiting adaptor proteins GRB2 and SHC to trigger the SOS-RAS-RAF-MEK-ERK cascade, promoting proliferation. Parallel signaling through PI3K-AKT enhances survival, while STAT3 activation downstream of JAK modulates transcription. EGFR also forms heterodimers with ErbB2/HER2, ErbB3, and ErbB4, and is negatively regulated by CBL-mediated ubiquitination and SRC kinase modulation.
In B16 melanoma, EGFR signaling contributes to proliferation, survival, migration, and may influence immune modulation. Egfr knockout ablates ligand-induced downstream effector activation, allowing precise dissection of EGFR-dependent phenotypes. This model is particularly valuable for studying EGFR??s role in melanoma aggressiveness and metastasis, and for evaluating EGFR-targeted therapies and resistance mechanisms in a syngeneic, immunocompetent setting.
This knockout cell line supports diverse applications, including mechanistic studies of EGFR in melanoma progression, high-throughput screening of EGFR-targeted inhibitors or biologics, and investigation of therapy resistance. In syngeneic mouse models, it enables assessment of how tumor-intrinsic EGFR loss shapes anti-tumor immunity. Representative assays encompass western blotting for phospho-ERK and phospho-AKT, MTT proliferation assays, transwell migration/invasion assays, Annexin V apoptosis detection, RNA-seq transcriptomic profiling, and flow cytometry to validate EGFR surface loss. For further information, please contact Ascent Research.
