Our broad portfolio consists of multiplex panels that allow you to choose, within the panel, analytes that best meet your needs. On a separate tab you can choose the premixed cytokine format or a single plex kit.
Cell Signaling Kits & MAPmates™
Choose fixed kits that allow you to explore entire pathways or processes. Or design your own kits by choosing single plex MAPmates™, following the provided guidelines.
The following MAPmates™ should not be plexed together:
-MAPmates™ that require a different assay buffer
-Phospho-specific and total MAPmate™ pairs, e.g. total GSK3β and GSK3β (Ser 9)
-PanTyr and site-specific MAPmates™, e.g. Phospho-EGF Receptor and phospho-STAT1 (Tyr701)
-More than 1 phospho-MAPmate™ for a single target (Akt, STAT3)
-GAPDH and β-Tubulin cannot be plexed with kits or MAPmates™ containing panTyr
.
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Select A Species, Panel Type, Kit or Sample Type
To begin designing your MILLIPLEX® MAP kit select a species, a panel type or kit of interest.
Custom Premix Selecting "Custom Premix" option means that all of the beads you have chosen will be premixed in manufacturing before the kit is sent to you.
If you have chosen panel analytes and then choose a premix or single plex kit, you will lose that customization.
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96-Well Plate
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Add Additional Reagents (Buffer and Detection Kit is required for use with MAPmates)
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
Space Saver Option Customers purchasing multiple kits may choose to save storage space by eliminating the kit packaging and receiving their multiplex assay components in plastic bags for more compact storage.
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Description
Overview
A selective antagonist of G protein-coupled receptor 55 (GPR55) that blocks lipid L-a-lysophosphatidylinositol (LPI, Cat. No. 440153)-induced GPR55 activation (IC50 = 1 µM) and downstream effects in HEK293 cells. Also shown to block the agonistic effect of LPI on GPR55- expressing yeast cells (~10 µM). Inhibits LPI-induced Ca2+ mobilization and ERK1/2 phosphorylation in HEK-GPR55 and HEK-CB1 cells. However, it does not affect basal Ca2+ mobilization and ERK1/2 activity. Blocks the GPR55-mediated NFAT and NF-kB activation and their nuclear translocation in HEK-GPR55 cells. Diminishes LPI-induced wound healing in GPR55-expressing primary human lung microvascular endothelial cells and reverses LPI-inhibited platelet aggregation (~10 µM). Also reported to inhibit the activity of phosphodiesterases PDE3A and PDE4B (pIC50 = 5 and 4.8, respectively).
Kargl, J., et al, 2013. J. Pharmacol. Exp. Ther.346, 54.
Data Sheet
Note that this data sheet is not lot-specific and is representative of the current specifications for this product. Please consult the vial label and the certificate of analysis for information on specific lots. Also note that shipping conditions may differ from storage conditions.
A selective antagonist of G protein-coupled receptor 55 (GPR55) that blocks lipid L-a-lysophosphatidylinositol (LPI, Cat. No. 440153)-induced GPR55 activation (IC50 = 1 µM) and downstream effects in HEK293 cells. Also shown to block the agonistic effect of LPI on GPR55- expressing yeast cells (~10 µM). Inhibits LPI-induced Ca2+ mobilization and ERK1/2 phosphorylation in HEK-GPR55 and HEK-CB1 cells. However, it does not affect basal Ca2+ mobilization and ERK1/2 activity. Blocks the GPR55-mediated NFAT and NF-kB activation and their nuclear translocation in HEK-GPR55 cells. Diminishes LPI-induced wound healing in GPR55-expressing primary human lung microvascular endothelial cells and reverses LPI-inhibited platelet aggregation (~10 µM). Also reported to inhibit the activity of phosphodiesterases PDE3A and PDE4B (pIC50 = 5 and 4.8, respectively).
Form
Off-white powder
Intert gas (Yes/No)
Packaged under inert gas
Chemical formula
C₂₅H₁₉N₃O₄
Structure formula
Purity
≥99% by HPLC
Solubility
DMSO (100 mg/ml)
Storage
Protect from light
+2°C to +8°C
Do Not Freeze
Ok to freeze
Special Instructions
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Toxicity
Standard Handling
References
Kargl, J., et al, 2013. J. Pharmacol. Exp. Ther.346, 54.
