CD27/NF-kB Reporter-Jurkat Recombinant Cell Line

T6504

CD16-NFAT Luciferase Reporter Jurkat Cell Line

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ABC-RC098D

CD27/NF-kB Report Cell Line-Jurkat

Recombinant Jurkat T cell expressing firefly luciferase gene under the control of NF-kB response elements with constitutive expression of human CD27 (also known as Tumor Necrosis Factor Receptor Superfamily Member 7, TNFRSF7, and T14, Genbank Accession #BC012160)

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ABC-RC0084

Human CD40/NF-kB Reporter Cell Line

The CD40 NF-kB Reporter HEK293 Stable Cell Line is ideal for High Throughput Screening (HTS) to identify potential CD40 agonistic monoclonal antibodies and CD40-specific inhibitors.

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78363

B2M Knockout NFAT Luciferase Reporter Jurkat Cell Line

B2M (Beta-2-Microglobulin) has been genetically removed by CRISPR/Cas9 genome editing from NFAT Luciferase Reporter Jurkat cells. Expression of the firefly luciferase gene is driven by NFAT response elements located upstream of the minimal TATA promoter. Activation of the NFAT signaling pathway in these cells can be monitored by measuring luciferase activity.

16792.5 €

78556

TCR Knockout NFAT-Luciferase Reporter Jurkat Cell Line

This cell line is a knockout of TCR (T Cell Receptor). The TRAC (T-Cell Receptor Alpha Constant) and TRBC1 (T-Cell Receptor Beta Constant 1) domains of the TCRα/β chains were genetically removed by CRISPR/Cas9 genome editing from recombinant Jurkat cells stably expressing the firefly luciferase gene under the control of NFAT response elements.This cell line has been functionally validated and does not respond to anti-CD3 agonist antibodies, as opposed to parental NFAT-Luciferase Reporter Jurkat cells (BPS Bioscience #60621).

18457.5 €

ABC-RC0024

Human NFAT Luciferase Reporter Cell Line- Jurkat T

Human NFAT Luciferase Reporter Cell Line- Jurkat T is derived from human T lymphocyte,and stably express firefly luciferase reporter gene under the control of NFAT response element. This cell line is an ideal cellular model for monitoring the activation of Calcium Signaling Pathway triggered by stimuli treatment, enforced gene expression and gene knockdown.

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