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MC3R-CRE-BLA CHO-K1 CELLS 1 KIT,K1744,Invitrogen

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订货号 6UE5565
品牌型号 Invitrogen K1744
货期 询货期
最小订货量 1套
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产品介绍 Product Description
规格
Accession Number: NM_019888.2
Assay Entry: Cell-based beta lactamase reporter gene
Cell Line: CHO-K1
Cell State: Dividing Cells
Druggable Target: GPCRs
Gene Symbol: MC3R
Population Status: Single Cell Clone Origin
Product Line: GeneBLAzer®
Reporter Gene: BLA (Beta-Lactamase)
System Type: GeneBLAzer™
Target Entry: MC3R
Technique: FRET
Detection Method: Fluorescent
储存
Contents:
K1744 GeneBLAzer® MC3R CRE-bla CHO-K1 DA cells
(LiveBLAzer™-FRET B⁄G Loading Kit, Solution D and other materials are required separately; please refer to the protocol).
Includes:
• GeneBLAzer® MC3R CRE-bla CHO-K1 cells
• GeneBLAzer® MC3R CRE-bla CHO-K1 Assay Protocol
• Certificate of Analysis

Storage:
The GeneBLAzer® MC3R CRE-bla CHO-K1cells are shipped on dry ice and should be stored in liquid nitrogen immediately upon receipt.
描述

GeneBLAzer® MC3R CRE-bla CHO-K1 cells contain the human Melanocortin Receptor 3 (MC3R) stably integrated into the CellSensor® CRE-bla CHO-K1 cell line. CellSensor® CRE-bla CHO-K1 cells (Cat. no. K1535) contain a beta-lactamase reporter gene under control of the Cyclic AMP Response Element (CRE) response element.

The GeneBLAzer® MC3R CRE-bla CHO-K1 DA cells are functionally validated for Z' and EC50 concentrations of NDP-α-MSH. In addition, GeneBLAzer® MC3R CRE-bla CHO-K1 DA cells have been tested for assay performance under variable conditions. These data are found in the Validation & Assay Performance Summary.

The melanocortin-3 receptor (MC3R) is primarily expressed in the hypothalamus, and plays an important role in the regulation of energy homeostasis. MC3R recognizes all of the melanocortin peptides, and notably binds - -MSH with greater affinity than the other melanocortin receptors. MC3R-deficient (MC3R-/-) mice demonstrate increased fat mass, higher feeding efficiency, and reduced lean body mass. To date only one mutation of MC3R has been identified to be associated with human obesity. Functional analysis of this mutation indicated a complete loss of agonist-mediated receptor activation.

For Academic pricing please login or contact us at discoverysciences@invitrogen.com.

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