EGR1 Promoter Luciferase Reporter Lentivirus

Catalog #
78664
$860 *
Size: 500 µl x 2
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Description

The Early growth response 1 (EGR1, also known as ZNF268 or NGFi-A) Promoter Luciferase Reporter Lentiviruses are replication incompetent, HIV-based, VSV-G pseudotyped lentiviral particles that are ready to be transduced into almost all types of mammalian cells, including primary and non-dividing cells. The particles contain a firefly luciferase gene driven by the human EGR1 promoter (~1.3 kb, Figure 1). After transduction, activation of the EGR1 promoter in the target cells can be monitored by measuring the luciferase activity. 

Figure 1. Schematic of the lenti-vector used to generate the EGR1 Promoter Luciferase Reporter Lentivirus.

Product Info
Storage and Usage
Citations
Supplied As
Two vials (500 µl x 2) of lentivirus at a titer >107 TU/ml. The titer will vary with each lot; the exact value will be provided with each shipment.
Materials Required But Not Supplied
Name Ordering Information
Phorbol 12-Myristate 13-Acetate (PMA) LC Laboratories #P-1680
Recombinant human epidermal growth factor (EGF) BPS Bioscience #90201
HEK293 growth medium or use Thaw Medium 1 BPS Bioscience #60187
Assay Medium 1D BPS Bioscience #78745
Polybrene Millipore #TR-1003-G
Formulation

The lentivirus particles were produced from HEK293T cells. They are supplied in cell culture medium containing 90% DMEM + 10% FBS.

Background

Early growth response factor 1 (EGR1) is a member of the EGR family and an important transcription factor. It contains an activation regulatory region, a repressive regulatory region, and three Cys2-His2 subclass zinc finger structures, all recognizing and binding target genes and regulating their transcription. Widely expressed in many different cell types, EGR1 is important in many physiological processes, including cell proliferation and inflammatory factors. EGR1 is a key molecule implicated in many signaling pathways and can act as a tumor suppressor to help monitor DNA damage. It can also promote tumor cell apoptosis and enhance the anticancer effects of radiotherapy and chemotherapy. Alternatively, increased EGR1 expression in hypoxic microenvironments will maintain tumor cell survival and proliferation. Researching the mechanisms of action of EGR1 can help study potential cancer therapies and new cancer treatment studies.