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Transfected Stable Cell Lines

Human ETV6 NTRK2 (G639R) BAF3 Cell Line

  • For research use only

Cat No.

ABC-X0007C
Product Type

Overexpression Stable Cell Lines
Cell Type

Lymphocyte
Species

Human
Host Cell

BAF3
Source Organ

Lymphatic
Disease

Normal
Storage

Liquid Nitrogen

The ETV6-NTRK2 (G639R) BAF3 cell line provides a stable gene overexpression model for malignant tumor research. Discover our custom services.

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  • Human ETV6 NTRK2 (G639R) BAF3 Cell Line
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Home | Transfected Stable Cell Lines | Overexpression Stable Cell Lines | Human ETV6 NTRK2 (G639R) BAF3 Cell Line

Description

Human ETV6-NTRK2 (G639R) BAF3 Cell Line is a genetically engineered model derived from selected murine Ba/F3 parental cell line based on customers’ requirement. ETV6-NTRK2 (G639R) BAF3 fusion cell line is generated by stable integration of exogenous human ETV6-NTRK2 fusion gene harboring the G639R point mutation into Ba/F3 host cells using our optimized transduction of lentiviral vectors.ETV6-NTRK2 fusions and their kinase-activating mutations are implicated in various malignancies, including congenital fibrosarcoma, leukemia, and thyroid carcinoma. AcceGen offers generation of stable overexpression and fusion gene cell lines targeting any gene or mutation of your interest. Polyclonal or monoclonal is optional based on customers’ research needs.

Species

Human
Cat.No

ABC-X0007C
Product Category

Transfected Stable Cell Lines
Size/Quantity

1 vial
Cell Type

Lymphocyte
Growth Mode

Suspension
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
Quality Control

All cells test negative for mycoplasma, bacteria, yeast, and fungi.

Application

  • The Human ETV6 NTRK2 (G639R) BAF3 Cell Line provides a functional model for exploring the role of mutant NTRK2 fusion proteins in cancer pathogenesis and drug response. The ETV6-NTRK2 fusion, particularly with the G639R point mutation, has been associated with oncogenic transformation and therapeutic resistance. This model supports high-throughput screening of TRK inhibitors, mechanistic studies of aberrant TRK signaling, and investigation of mutation-driven resistance to targeted therapies in hematologic and solid tumors.

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High Viability
To succeed in cell culture
Precision and Reliability
To support a consistent result
Customization Options
Tailed to your research

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