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48-680MAG

Millipore

MILLIPLEX MAP Multi-Pathway Magnetic Bead 9-Plex - Cell Signaling Multiplex Assay

Synonym(s):

ERK Cell Signaling Assay, Luminex® Cell Signaling Assay, Millipore Cell Signaling Assay

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About This Item

UNSPSC Code:
12161503
eCl@ss:
32161000
NACRES:
NA.47

species reactivity

human

Quality Level

manufacturer/tradename

Milliplex®

technique(s)

multiplexing: suitable

detection method

fluorometric (Luminex xMAP)

storage temp.

2-8°C

General description

The Milliplex® MAP 9-plex Multi-Pathway Signaling Magnetic Bead kit, phosphoprotein, is used to detect changes in phosphorylated ERK/MAP kinase 1/2 (Thr185/Tyr187), Akt (Ser473), STAT3 (Ser727), JNK (Thr183/Tyr185), p70S6K (Thr412), NFkB (Ser536), STAT5A/B (Tyr694/699), CREB (Ser133), and p38 (Thr180/Tyr182) in cell lysates using the Luminex® xMAP® technology. The detection assay is a rapid, convenient alternative to Western Blotting and immunoprecipitation procedures. Each kit has sufficient reagents for one 96-well plate assay.

Specificity

Cross-reactivity between the antibodies and any of the other analytes in this panel is non-detectable or negligible.

Application

Analyze a cell signaling panel using this kit. The analytes available for the cell signaling multiplex assay kit are: CREB (pS133), ERK (pT185/pY187), NFκB (pS536), JNK (pT183/pY185), p38 (Thr180/Tyr182), p70S6K (Thr412), STAT3 (pS727), STAT5A/B (pY694/699), Akt (pS473).
Research Category
Cell Signaling
Research Sub Category
Oncology
Used to detect/quantify:CREB (pS133)|ERK (pT185/pY187)|NFκB (pS536)|JNK (pT183/pY185)|p38 (Thr180/Tyr182)|p70S6K (Thr412)|STAT3 (pS727)|STAT5A/B (pY694/699)|Akt (pS473)

Storage and Stability

Recommended storage for kit components is 2 - 8°C

Legal Information

Luminex is a registered trademark of Luminex Corp
MILLIPLEX is a registered trademark of Merck KGaA, Darmstadt, Germany
xMAP is a registered trademark of Luminex Corp

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial

Signal Word

Danger

Hazard Statements

Hazard Classifications

Acute Tox. 4 Oral - Aquatic Acute 1 - Aquatic Chronic 2 - Eye Dam. 1 - Skin Irrit. 2

Storage Class Code

10 - Combustible liquids

Regulatory Information

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Certificates of Analysis (COA)

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Lee A Denson et al.
Inflammatory bowel diseases, 25(3), 547-560 (2018-08-21)
Granulocyte-macrophage colony-stimulating factor auto-antibodies (GMAbs) suppress neutrophil-extrinsic GM-CSF signaling and increase risk for stricturing behavior in Crohn's disease (CD). We aimed to define clinical, genomic, and functional associations with neutrophil-intrinsic GM-CSF signaling. Missense mutations in CSF2RA, CSF2RB, JAK2, STAT5A, and
Christopher P Stanley et al.
Pharmacological research, 113(Pt A), 356-363 (2016-10-21)
The endocannabinoid anandamide (AEA) causes vasorelaxation in animal studies. Although circulating AEA levels are increased in many pathologies, little is known about its vascular effects in humans. The aim of this work was to characterise the effects of AEA in
Fernanda Ursoli Ferreira et al.
International journal of molecular sciences, 20(3) (2019-01-27)
The endothelial-to-mesenchymal transition (EndMT) is a biological process where endothelial cells (ECs) acquire a fibroblastic phenotype after concomitant loss of the apical-basal polarity and intercellular junction proteins. This process is critical to embryonic development and is involved in diseases such
Anna Coulibaly et al.
Scientific reports, 11(1), 7023-7023 (2021-03-31)
Natural killer (NK) cells mediate innate host defense against microbial infection and cancer. Hypoxia and low glucose are characteristic for these tissue lesions but do not affect early interferon (IFN) γ and CC chemokine release by interleukin 15 (IL-15) primed
Belinda I Gómez et al.
The Journal of surgical research, 248, 28-37 (2019-12-17)
The endothelial glycocalyx controls vascular permeability, cellular signaling, blood-endothelial cell adhesion, extravasation, and transmission of shear stress signals. Burn injury compromises integrity of this layer increasing vascular permeability, which is further exacerbated by large volumes of (intravenous) crystalloids. We have

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