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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It is well known that biosynthesis of glycans takes place in organ- and tissue-specific manners and glycan expression is controlled by various factors including glycosyltransferases. The expression mechanism of glycosyltransferases, however, is poorly understood. Here we investigated the expression mechanism of a brain-specific glycosyltransferase, GnT-IX (N-acetylglucosaminyltransferase IX, also designated as GnT-Vb), which synthesizes branched O-mannose glycan. Using an epigenetic approach, we revealed that the genomic region around the transcriptional start site of the GnT-IX gene was highly associated with active chromatin histone marks in a neural cell-specific manner, indicating that brain-specific GnT-IX expression is under control of an epigenetic "histone code." By EMSA and ChIP analyses we identified two regulatory proteins, NeuroD1 and CTCF that bind to and activate the GnT-IX promoter. We also revealed that GnT-IX expression was suppressed in CTCF- and NeuroD1-depleted cells, indicating that a NeuroD1- and CTCF-dependent epigenetic mechanism governs brain-specific GnT-IX expression. Several other neural glycosyltransferase genes are also found to be regulated by epigenetic histone modifications. This is the first report demonstrating a molecular mechanism at the chromatin level underlying tissue-specific glycan expression.