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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Since individual cells from freshly isolated white adipose tissue (WAT) exhibit variable levels of fat accumulation, we attempted to determine which factor(s) cause this variation. We used primary WAT cells from adult mice and the mouse 3T3-L1 cell-line of preadipocytes for these studies. Cells were labeled with BODIPY (boron-dipyrromethene) lipid probe, a marker for fat accumulation in live cells, and sorted on a fluorescence-activated cell sorter into two populations exhibiting low or high BODIPY fluorescence intensity. After more than 12 doublings as dedifferentiated cells in growth medium, the sorted populations were exposed to adipogenic medium for 7 days and analyzed for BODIPY accumulation and mRNA expression of adipogenic markers. WAT-derived cells initially sorted to have low or high BODIPY fluorescence intensity maintained a similar low or high lipid phenotype after redifferentiation. Cell surface TSH receptor expression, which is known to increase when preadipocytes are differentiated, correlated with BODIPY staining in all states. mRNA levels of Pparγ, Srebp1c, aP2, and Pref1, key regulators of adipogenesis, and leptin, Glut4, Fasn, and Tshr, markers of adipocyte differentiation, correlated with the levels of fat accumulation. Overexpression of Pparγ in 3T3-L1 cells, as expected, caused cells from low- and high-BODIPY populations to accumulate more fat. More importantly, prior to differentiation, the endogenous Pparγ promoter exhibited higher levels of acetylated histone H3, an activatory modification, in high-BODIPY- compared with low-BODIPY-derived populations. We conclude that fat accumulation is a heritable trait in WAT and that epigenetic modification on the Pparγ promoter contributes to this heritability.
Although acute respiratory infections (ARIs) are a major cause of child morbidity and mortality in Southern Brazil, little information is available on their seasonality and viral etiology. This study was conducted on children under 5 years of age with ARI to assess viral etiology in the State of Rio Grande do Sul, from 1990 to 1992. A total of 862 nasopharyngeal secretion (NPS) samples were tested using indirect immunofluorescence. The results showed that 316 (36.6%) NPS samples were positive: 26.2% for RSV, 6% for adenovirus, 1.7% for influenza viruses, 1.5% for parainfluenza viruses, and 1.2% for mixed infection. The mean viral prevalence rates in out-patient services, emergency wards, and in-patient hospital wards were 26.7%, 53% and 42.3%, respectively. Respiratory syncytial virus (RSV) and adenovirus accounted for 91.4 % of the viral diagnoses. RSV was more frequent in children under one year of age at the three levels of health care and was prevalent in infants under six months. Adenovirus was the most prevalent pathogen in hospitalized children, in 1992. Influenza A virus showed an increased prevalence with age among out-patient children. This study shows the annual occurrence of viral respiratory infections in the coldest months, with a significant annual variation in the frequency of RSV infection.
Porous polyethylene (Medpor(®)) is frequently used in craniofacial reconstructive surgery. The successful incorporation of this alloplastic biomaterial depends on adequate vascularization. Here, we analyzed whether the early vascularization of porous polyethylene can be accelerated by vitalization with human chondrocytes. For this purpose, small polyethylene samples were coated with platelet-rich plasma (PRP) or a suspension of PRP and human chondrocytes. Uncoated polyethylene samples served as controls. Subsequently, the samples were implanted into the dorsal skinfold chamber of CD-1 nude mice to repetitively analyze their vascularization and biocompatibility by means of intravital fluorescence microscopy. PRP-chondrocyte-coated polyethylene exhibited an accelerated and improved vascularization when compared with the other two groups. This was indicated by a significantly higher functional capillary density of the microvascular network developing around the implants. Moreover, a leukocyte-endothelial cell interaction was found in a physiological range at the implantation site of all three groups, demonstrating that the vitalization with PRP and chondrocytes did not affect the good biocompatibility of the alloplastic material. Additional histological, immunohistochemical, and in situ hybridization analyses revealed that the chondrocytes formed a bioprotective tissue layer, which prevented the accumulation of macrophages and foreign body giant cells on the polyethylene surface. These findings clearly indicate that vitalization of polyethylene with chondrocytes promotes early implant vascularization and incorporation into the host tissue and, thus, may be a promising approach that prevents postoperative complications such as implant extrusion, migration, and infection.