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.
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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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The effects of organophosphate pesticides on human placenta remain poorly investigated although an increased risk of pregnancy alterations has been reported in women chronically exposed to these pesticides. Here, we have addressed whether chlorpyrifos (CPF) modifies the expression of genes relevant for placental function. Human placental JEG-3 cells were exposed to increasing CPF concentrations up to 100 μM for 24 and 48 h and cell viability, mRNA, protein and hormone levels were analyzed. Quantitative RT-PCR assays revealed that CPF increased the expression of ABCG2, GCM1 and, even more significantly, βhCG mRNAs in conditions where cell viability and morphology were not compromised. In addition, βhCG protein synthesis and secretion were time-dependently augmented. Present results may reflect a CPF nocive effect on placenta cells or a placental-defense mechanism to preserve its function. These novel CPF trophoblast target genes should be considered in future studies of pregnancy outcomes associated with in vivo exposures.