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Transfected Stable Cell Lines

Human MPL CALR BAF3 Cell Line

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Species

Human

Cat.No

ABC-X0008C

Quality Control

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

Product Category Transfected Stable Cell Lines
Size/Quantity

1 vial

Cell Type

Lymphocytes

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 MPL CALR BAF3 Cell Line is a genetically engineered model derived from the murine pro-B cell line BAF3, customized according to specific research needs. The cell line was developed through stable co-expression of exogenous human MPL (myeloproliferative leukemia virus oncogene) and mutant CALR (calreticulin) in BAF3 host cells using lentiviral vector-based transduction. Dual overexpression is validated at the transcript level by qRT-PCR.
Target
The MPL gene encodes a transmembrane receptor for thrombopoietin (TPO), primarily involved in hematopoietic stem cell maintenance and megakaryocyte differentiation via JAK-STAT signaling. Mutations in the CALR gene, often found in exon 9, result in a frameshift that produces a novel C-terminal peptide capable of aberrantly activating MPL. Co-expression of mutant CALR and MPL leads to constitutive, ligand-independent receptor activation, driving proliferation and survival of hematopoietic cells. This interaction underlies the pathogenesis of certain myeloproliferative neoplasms (MPNs), such as essential thrombocythemia and primary myelofibrosis. AcceGen offers generation of stable 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 Human MPL CALR BAF3 Cell Line serves as a robust model for studying the pathogenic mechanisms of CALR-mutant myeloproliferative disorders and their dependence on MPL signaling. It facilitates investigation of downstream JAK-STAT activation, cytokine independence, and therapeutic sensitivity to JAK inhibitors such as ruxolitinib. This model is widely used in drug screening platforms for selective inhibitors of mutant CALR-MPL interactions, supporting both target validation and mechanistic studies in hematologic malignancies.

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

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