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Transfected Stable Cell Lines

Human NRAS (G13C) BAF3 Cell Line

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Home | Transfected Stable Cell Lines | Overexpression Stable Cell Lines | Human NRAS (G13C) BAF3 Cell Line
Species

Human
Cat.No

ABC-X0003C
Quality Control

All cells test negative for mycoplasma, bacteria, yeast, and fungi.
Product Category Transfected Stable Cell Lines
Size/Quantity

1 vial
Cell Type

Lymphocyte
Shipping Info

Dry Ice
Growth Conditions

37 °C, 5% CO₂
Source Organ

Lymphatic
Disease

Normal
Biosafety Level

1
Storage

Liquid Nitrogen
Product Type

Overexpression Stable Cell Lines
Host Cell

BAF3

Description

Human NRAS (G13C) BAF3 Cell Line is a genetically engineered model derived from selected murine Ba/F3 parental cell line based on customers’ requirement. NRAS (G13C) BAF3 mutant cell line is generated by stable integration of exogenous human NRAS gene harboring the G13C point mutation into Ba/F3 host cells using our optimized transduction of lentiviral vectors.
Target
The NRAS gene encodes a small GTPase that regulates cellular proliferation, differentiation, and survival through the RAS/RAF/MEK/ERK and PI3K/AKT signaling pathways. The G13C mutation is an activating hotspot alteration within the GTP-binding domain, resulting in impaired GTP hydrolysis and constitutive RAS pathway activation. This mutation is implicated in various human cancers, including hematologic malignancies and melanoma. It is associated with enhanced tumorigenicity and resistance to certain targeted therapies. AcceGen offers generation of stable mutation-specific or overexpression cell lines targeting any gene of your interest. Polyclonal or monoclonal is optional based on customers’ research needs.

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Application

  • For research use only

  • The NRAS (G13C) BAF3 Cell Line serves as a powerful tool to investigate RAS-driven oncogenic mechanisms and therapeutic interventions. This model enables mechanistic studies of mutant NRAS signaling, IL-3-independent survival, and drug resistance in hematopoietic cell models. It is utilized for high-throughput screening of RAS-targeted inhibitors, synthetic lethality approaches, and evaluation of combination therapies with MEK or PI3K inhibitors.

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