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MELK Signaling Pathway Assay (CAT#: STEM-MB-0311-WXH)

Introduction

MELK is a Ser/Thr protein kinase whose high expression can inhibit the differentiation and apoptosis of some stem cells and tumor cells and promote their proliferation. In a variety of tumor cells, MELK can be inhibited by siRNA to reduce its protein expression. MELK was found to be a new potential target for tumor therapy. The multiple functions of MELK affect numerous proteins and signaling pathways through protein-protein interactions.




Principle

MELK physically interacts with apoptotic signal-regulated kinase 1 (ASK1), whose activity is positively or negatively regulated by its interacting molecules. As an upstream kinase of ASK1, MELK phosphorylates threonine 838 in the activation ring of human ASK1, thus stimulating the kinase activity of ASK1. This interaction enhances JNK-mediated transduction and H2O2-induced apoptosis. MELK also physically interacts with p53 and enhances p53-dependent apoptosis and cell cycle cessation. Therefore, MELK is thought to be a regulator of cell proliferation, division, and apoptosis.

Applications

Study the regulatory mechanism of MELK signaling pathway in medicine
Study the impact of each clinical virus on the MELK signaling pathway
Study the effect of drugs or therapies on the MELK signaling pathway

Procedure

• Luminex Multiplex Assay
• Enzyme-linked immunosorbent assay (ELISA)
• Flow cytometry (FACS analysis) technology

Notes

Detectable targets: PKR, TLR3, IAPs, tBID, SODD, Bad, Bcl-xl, ISGF3, TRAF-2, FADD, APAF-1, BID, FADD, IRF7, Mda-5, NFκB, RIG-1, TRAF3, GAS, IRF9, MEKK1, p38, RIP1, TRAF5, Histone-H3, IRF5, MEK3, p38MAPK, SH2, TRAF6, RIP1, IRS1, MEK6, p50, SLP76, TRAM, PIDD, IRS2, MSK1, p65, Tak1, TRIF, IPS-1, mTOR, MSK2, PI3K, TBK1, Vav, BAK, Bax, ISRE, MYD88, Rac1, TLR4

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