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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Nitric oxide (NO) has major physiological and cellular effects on muscle growth, repair, and function. In most muscle biopsies from humans with myopathies, sarcolemma-localized neuronal nitric oxide synthase (nNOS) is either reduced or not detected, particularly in dystrophin-deficient Duchenne muscular dystrophy (DMD). Abnormal NO signaling at the sarcolemmal level is integrally involved in the pathogenesis and accounts, at least in part, for the muscle weakness of DMD. Dystrophic muscle fibers exhibit an increased susceptibility to contraction-induced membrane damage. Muscle relaxants function to prevent muscle wasting by decreasing nerve impulses and reducing calcium influx that regulates tensing or tightening of muscle fibers. We have recently developed a new class of nitric esters that combines the pharmacological functions of NO and muscle relaxation. Here, we report the synthesis and properties of the nitric ester (MMPN) of 2-methyl-2-n-propyl-1,3-propanediol (MPP) and its effect in mdx dystrophic mice, a murine model of DMD. MMPN produced significant improvements in biochemical, pathological, and functional phenotypes in the mouse model. The endurance of exercise was extended by 47% in time to exhaustion and 84% in running distance. Serum CK level was decreased by 30%. Additionally, MMPN decreased intracellular free calcium concentration without causing skeletal muscle weakness. No hepatic or renal toxicities were observed during the study. Our investigations unveil a potential new treatment for muscular diseases.