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IRF1 BLA HEL CELLS KIT,K1647,Invitrogen

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订货号 2KD2381
品牌型号 Invitrogen K1647
货期 询货期
最小订货量 1套
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产品介绍 Product Description
规格
Assay Entry: Cell-based beta lactamase reporter gene
Cell State: Dividing Cells
Druggable Target: Cytokines, Signaling Pathway
Product Line: CellSensor™
System Type: CellSensor™
Target Entry: JAK/STAT pathway, JAK2 (V617F), STAT5
储存
CellSensor® Cell Lines are shipped on dry ice. Store in liquid nitrogen immediately upon receipt, or thaw for immediate use.
描述

Jak/Stat signaling pathways play essential roles in the cellular responses to distinct cytokines. One of Jak/Stat pathways, Jak2/Stat5, mediates cell proliferation in response to Interleukin-3 (IL-3), prolactin, erythropoietin (Epo), and granulocyte-macrophage colony stimulating factor (GM-CSF). JAK2 gene knock-out causes embryonic lethality due to defective erythropoiesis, suggesting the Jak2/Stat5 pathway plays important role in red blood cell formation. Recent discovery of activating mutation in JAK2 (V617F) present in high percentage of myeloproliferative disease (MPD) patients suggests Jak2/Stat5 pathway to be the potential therapeutic target for certain forms of MPD. The activated transcription factor Stat5 dimers recognize and bind to a specific palindromic DNA sequence found in the promoter region of β-casein, interferon regulatory factor-1 (irf-1) and a number of other genes. The CellSensor® irf1-bla HEL cell line contains a beta-lactamase reporter gene under control of the interferon regulatory factor-1 (irf1) response element stably integrated into HEL cells. HEL cells are a human erythroleukemia cell line that is growth factor independent and contains a endogenous homozygous JAK2V617F mutation. This cell line validated for IC50 and Z'-Factor under optimized conditions using Jak Inhibitor 1 (Figure 1). This cell line has also been tested under variable experimental conditions, including DMSO concentration, cell number, stimulation time, and substrate loading time. Academic and non-profit customers, please inquire for special pricing.

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