Based on Luminex technology platform, Creative Proteomics provides analysis services for key targets of MELK signaling pathway.
(Pengfei Jiang, et al., 2019)Maternal Embryonic Leucine Zipper Kinase (MELK) is initially cloned in oocytes and detected both in normal tissues and in cancer cells. MELK serves as a marker for selfrenewing multipotent neural progenitors (MNPs) in culturesderived from the developing forebrain and in transgenicmice. Overexpression of MELK enhances (whereas knock-down diminishes) the ability to generate neurospheresfrom MNPs, indicating a function in self-renewal. MELK down-regulation disrupts the production of neurogenic MNP from glial fibrillary acidic protein (GFAP) positiveprogenitors in vitro. MELK expression in MNP is cell cycleregulated and inhibition of MELK expression down-regu-lates the expression of B-myb, which is shown to also me-diate MNP proliferation. These indicate that MELK is necessary for proliferation of embryonic and postnatal MNP and suggest that it regulates the transition from GFAP-expressing progenitors to rapid amplifying progenitors in the postnatal brain.
MELK is upregulated in a variety of human tumors, where it contributes to malignant phenotype and correlates with a poor prognosis.
As a regulator of intracellular signaling, Melk affects various cellular and biological processes including cell cycle, cell proliferation, apoptosis, spliceosome assembly, gene expression, embryonic development, hematopoiesis and tumorigenesis. During these cellular processes, MELk works by binding to a number of proteins. In general, the interaction between various proteins and MELK is carcinogenic, and the overexpression of MELK in various cancers may be involved in the tumorigenic process.
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.
We provide Luminex technology for MELK signaling pathway analysis.
Luminex technology is a multifunctional liquid phase analysis platform developed on the basis of color microspheres, laser technology, applied fluid science and high-speed digital signal processing technology. The core is to encode polypropylene microspheres or magnetic microspheres with fluorescent dyes. By adjusting the different ratios of the two fluorescent dyes, up to 100 microspheres with different fluorescence spectra can be obtained. Antigen-antibody, enzyme-substrate, ligand-receptor binding reactions and nucleic acid hybridization reactions were performed on microspheres with different fluorescence codes. The microsphere coding and reporting fluorescence were analyzed qualitatively and quantitatively by laser detection.
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.
In addition to Luminex Multiplex Assay, Enzyme-linked immunosorbent assay (ELISA), Flow cytometry (FACS analysis) technology can also be provided to meet other customer needs.
Creative Proteomics has developed a signaling pathway target detection platform. We can provide detection services not only for apoptotic signaling pathways, but also for other signaling pathways. If you want to detect other targets, please contact us in advance and we will customize the service for you according to your requirements. Looking forward to working with you.