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Transfected Stable Cell Lines

Human PDGFRB (W566R) NIH/3T3 Cell Line

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Home | Transfected Stable Cell Lines | Overexpression Stable Cell Lines | Human PDGFRB (W566R) NIH/3T3 Cell Line
Species

Human
Cat.No

ABC-X0012C
Quality Control

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

1 vial
Cell Type

Fibroblast
Shipping Info

Dry Ice
Growth Conditions

37 °C, 5% CO₂
Source Organ

Embryo
Disease

Normal
Biosafety Level

1
Storage

Liquid Nitrogen
Product Type

Overexpression Stable Cell Lines
Host Cell

NIH/3T3

Description

Human PDGFRB (W566R) NIH/3T3 Cell Line is a genetically engineered model derived from selected murine NIH/3T3 parental cell line based on customers’ requirement. PDGFRB (W566R) NIH/3T3 mutant cell line is generated by stable integration of exogenous human PDGFRB gene harboring the W566R point mutation into NIH/3T3 host cells using our optimized transduction of lentiviral vectors.
Target
PDGFRB (platelet-derived growth factor receptor beta) is a receptor tyrosine kinase that regulates mesenchymal cell proliferation and migration. The W566R mutation, located in the juxtamembrane domain, has been shown to induce ligand-independent dimerization and constitutive receptor activation. Aberrant PDGFRB signaling is implicated in myeloproliferative neoplasms, gliomas, and soft tissue sarcomas. 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.

AcceGen Frozen Cells & Cell Lines 1 vial
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Application

  • For research use only

  • The PDGFRB (W566R) NIH/3T3 Cell Line serves as a powerful tool to investigate PDGFRB mutation-induced oncogenic transformation and targeted therapy development. This model enables mechanistic studies of receptor autophosphorylation, MAPK/PI3K pathway activation, and anchorage-independent growth. It is utilized for high-throughput drug screening and functional validation of PDGFRB inhibitors in solid and hematologic malignancies.

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