Transfected Stable Cell Lines

Human NRAS (G13R) NIH/3T3 Cell Line

  • For research use only

Cat No.

ABC-X0309C

Product Type

Overexpression Stable Cell Lines

Cell Type

Fibroblast

Species

Human

Host Cell

NIH/3T3

Source Organ

Embryo

Disease

Normal

Storage

Liquid Nitrogen

Human NRAS (G13R) NIH/3T3 Cell Line is engineered to study oncogenic NRAS mutations and their influence on cancer growth and therapeutic resistance.

Product Image

Description

Human NRAS (G13R) NIH/3T3 Cell Line expresses the G13R mutant NRAS gene in NIH/3T3 cells. This cell model is designed to mimic NRAS-driven transformation in vitro.
Target
The G13R mutation leads to constitutive activation of the NRAS protein, driving uncontrolled cell growth and survival. It is commonly associated with leukemia, melanoma, and colorectal cancer.
AcceGen offers generation of stable overexpression cell lines targeting any gene of your interest. Polyclonal or monoclonal is optional based on customers’ research needs.

Species

Human

Cat.No

ABC-X0309C

Product Category

Transfected Stable Cell Lines

Size/Quantity

1 vial

Cell Type

Fibroblast

Growth Mode

Adherent

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

Quality Control

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

Application

  • A valuable system for exploring NRAS-related oncogenesis, drug resistance mechanisms, and therapeutic targeting of Ras pathway mutations.

Inquiring Human NRAS (G13R) NIH/3T3 Cell Line

We know how valuable your research is to you, but are you wondering what you can expect to pay for quick accurate results every time? Fill out a request in the form below and we’ll get back to you within 24 hours with a quote.
High Viability
To succeed in cell culture
Precision and Reliability
To support a consistent result
Customization Options
Tailed to your research

Tags

AcceGen Scroll Top Button