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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This study sought to identify the relationship between fibroblast telomerase expression, myofibroblasts, and telomerase-mediated regulatory signals in idiopathic pulmonary fibrosis.Thirty-four surgical lung biopsies, which had been obtained from patients with idiopathic pulmonary fibrosis and histologically classified as usual interstitial pneumonia, were examined. Immunohistochemistry was used to evaluate fibroblast telomerase expression, myofibroblast α-smooth muscle actin expression and the tissue expression of inter leu kin-4, transforming growth factor-β, and basic fibroblast growth factor. The point-counting technique was used to quantify the expression of these markers in unaffected, collapsed, mural fibrosis, and honeycombing areas. The results were correlated to patient survival.Fibroblast telomerase expression and basic fibroblast growth factor tissue expression were higher in collapsed areas, whereas myofibroblast expression and interleukine-4 tissue expression were higher in areas of mural fibrosis. Transforming growth factor-β expression was higher in collapsed, mural fibrosis and honeycombing areas in comparison to unaffected areas. Positive correlations were found between basic fibroblast growth factor tissue expression and fibroblast telomerase expression and between interleukin-4 tissue expression and myofibroblast α-smooth muscle actin expression. Negative correlations were observed between interleukin-4 expression and basic fibroblast growth factor tissue expression in areas of mural fibrosis. Myofibroblast α-smooth muscle actin expression and interleukin-4 tissue expression in areas of mural fibrosis were negatively associated with patient survival.Fibroblast telomerase expression is higher in areas of early remodeling in lung tissues demonstrating typical interstitial pneumonia, whereas myofibroblast α-smooth muscle actin expression predominates in areas of late remodeling. These events seem to be regulated by basic fibroblast growth factor and interleukin-4 tissue expression, respectively.
A promising approach for the repair of osteochondral defects is the use of a scaffold with a well-defined cartilage-bone interface. In this study, we used a multiphasic composite scaffold with an upper collagen I fibre layer for articular cartilage repair, separated by a hydrophobic interface from a lower polylactic acid (PLA) part for bone repair. Focusing initially on the engineering of cartilage, the upper layer was seeded with human mesenchymal stem cells (hMSCs) suspended in a collagen I hydrogel for homogeneous cell distribution. The constructs were cultured in a defined chondrogenic differentiation medium supplemented with 10 ng/ml transforming growth factor-beta1 (TGFbeta1) or in DMEM with 10% fetal bovine serum as a control. After 3 weeks a slight contraction of the collagen I fibre layer was seen in the TGFbeta1-treated group. Furthermore, a homogeneous cell distribution and chondrogenic differentiation was achieved in the upper third of the collagen I fibre layer. In the TGFbeta1-treated group cells showed a chondrocyte-like appearance and were surrounded by a proteoglycan and collagen type II-rich extracellular matrix. Also, a high deposition of glycosaminoglycans could be measured in this group and RT-PCR analyses confirmed the induction of chondrogenesis, with the expression of cartilage-specific marker genes, such as aggrecan and collagen types II and X. This multiphasic composite scaffold with the cartilage layer on top might be a promising construct for the repair of osteochondral defects.
We have characterized the mouse carotid body (CB) with special attention to nicotinic, purinergic and dopaminergic receptors as well as the TASK-1 K(+)-channel. Mouse CB sections were stained immunohistochemically and visualized using fluorescent and confocal microscopy. The CB type 1 cells contained the alpha3 (n=8), alpha4 (n=7), alpha7 (n=4) and beta2 (n=3) nicotinic acetylcholine receptor (nAChR) subunits, the ATP-receptors P2X(2) (n=15) and P2X(3) (n=9), the dopamine D(2) receptor (n=9) and the TASK-1 K(+)-channel (n=7). Here we report the presence of alpha3, alpha4, alpha7 and beta2 nAChR subunits, the D(2) receptor and the TASK-1 K(+)-channel in the mouse CB. Also, we confirm the presence of the P2X(2) and P2X(3) receptors in mouse CB. Thus, we have localized nicotinergic, purinergic and dopaminergic receptors and the TASK-1 K(+)-channel on a protein level in one species. Our data are in line with the theory that the CB chemoreceptor cell hosts an orchestra of receptor systems that ultimately modulate the response to hypoxia.