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 wave-type African weakly electric fish Gymnarchus niloticus produces electric organ discharges (EODs) from an electric organ in the tail that is driven by a pacemaker complex in the medulla, which consists of a pacemaker nucleus, two lateral relay nuclei and a medial relay nucleus. The prepacemaker nucleus (PPn) in the area of the dorsal posterior nucleus of the thalamus projects exclusively to the pacemaker nucleus and is responsible for EOD interruption behavior. The goal of the present study is to test the existence of inhibition of the pacemaker nucleus by the PPn. Immunohistochemical results showed clear anti-GABA immunoreactive labeling of fibers and terminals in the pacemaker nucleus, but no apparent anti-glycine immunoreactivity anywhere in the pacemaker complex. GABA injection into the pacemaker nucleus could induce EOD interruptions that are comparable to the interruptions induced by glutamate injection into the PPn. Application of the GABA(A) receptor blocker bicuculline methiodide reversibly eliminated the effects of stimulation of the PPn. Thus the EOD interruption behavior in Gymnarchus is mediated through GABAergic inhibition of the pacemaker nucleus by the PPn.
The apolipoprotein ε4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and is associated with earlier age of onset. The incidence of spontaneous seizures has been reported to be increased in sporadic AD as well as in the early onset autosomal dominant forms of AD. We now report the emergence of a seizure phenotype in aged apolipoprotein E4 (apoE4) targeted replacement (TR) mice but not in age-matched apoE2 TR or apoE3 TR mice. Tonic-clonic seizures developed spontaneously after 5 months of age in apoE4 TR mice and are triggered by mild stress. Female mice had increased seizure penetrance compared to male mice, but had slightly reduced overall seizure severity. The majority of seizures were characterized by head and neck jerks, but 25% of aged apoE4 TR mice had more severe tonic-clonic seizures which occasionally progressed to tonic extension and death. Aged apoE4 TR mice progressed through pentylenetetrazol-induced seizure stages more rapidly than did apoE3 TR and apoE2 TR mice. Electroencephalographic (EEG) recordings revealed more frequent bursts of synchronous theta activity in the hippocampus of apoE4 TR mice than in apoE2 TR or apoE3 TR mice. Cortical EEG recordings also revealed sharp spikes and other abnormalities in apoE4 TR mice. Taken together, these findings demonstrate the emergence of an age-dependent seizure phenotype in old apoE4 TR mice in the absence of human amyloid-β peptide (Aβ) overexpression, suggesting increased central nervous system neural network excitability.