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 avian brainstem serves as a useful model to answer the question of how afferent activity influences the viability of target neurons. Approximately 20-30% of neurons in the avian cochlear nucleus, nucleus magnocellularis (NM) die following deafferentation (i.e., deafness produced by cochlea removal). Interestingly, Bcl-2 mRNA (but not protein) is upregulated in 20-30% of NM neurons following deafferentation. We have recently shown that chronic treatments of lithium upregulates the neuroprotective protein Bcl-2 and increases neuronal survival following deafferentation. The pathways leading to the upregulation of Bcl-2 expression following these two manipulations are unknown. The present experiments examine changes in glycogen synthase kinase-3 beta (Gsk-3beta), and transcription factors nuclear factor kappaB (NFkappaB), beta-catenin, and pCreb following lithium administration and following deafferentation. These molecules are known to be influenced by lithium and to regulate Bcl-2 expression in other model systems. Lithium decreased immunolabeling for Gsk-3beta and increased expression for all three transcription factors. Deafferentation, however, did not alter Gsk-3beta or NFkappaB, resulted in lower beta-catenin expression, but did increase pCreb immunoreactivity. While it is possible that pCreb is a common link in the regulation of Bcl-2 following these two manipulations, the timing and distribution of pCreb labeling suggests that it is not the sole determinant of Bcl-2 upregulation following deafferentation. It is likely that the regulation of Bcl-2 gene expression by lithium and by deafferentation involves different molecular pathways.