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Serine/threonine-protein kinase involved in various processes such as cell cycle regulation, self-renewal of stem cells, apoptosis and splicing regulation (By similarity). Additionally we are shipping MELK Antibodies (135) and MELK Proteins (14) and many more products for this protein.
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Study demonstrates that the interaction occurring between MELK and EZH2 (show EZH2 ELISA Kits) promotes self-proliferation and stemness.
In common culture conditions, the authors found that small molecule inhibition, genetic deletion, or acute depletion of MELK did not significantly affect cellular growth.
Synthesis of MCL1 (show MCL1 ELISA Kits), an antiapoptotic protein known to play a role in cancer cell survival during cell division, depends on the function of MELK-elF4B signaling.
Inhibition of MELK (genetically and pharmacologically) induces radiation sensitivity.
MELK is a host factor required for optimal uncoating of the HIV-1 core to promote viral cDNA synthesis.
Here, the authors report that mutagenizing MELK with CRISPR/Cas9 has no effect on the fitness of basal breast cancer cell lines or cell lines from six other cancer types. Cells that harbor null mutations in MELK exhibit wild-type doubling times, cytokinesis, and anchorage-independent growth.
MELK-inhibitor has a role in triple-negative breast cancer cells demonstrating context-dependent response with p53 (show TP53 ELISA Kits) as a key determinant
MELK is an oncogenic kinase involved in the pathogenesis and recurrence of hepatocellular carcinoma.
Inhibition or depletion of MELK reduced cell proliferation and anchorage-dependent and -independent growth in various ovarian cancer cell lines through a G2/M cell cycle arrest, eventually resulting in apoptosis.
Report IL11RA (show IL11RA ELISA Kits) and MELK amplification in gastric cancer cell lines and primary gastric adenocarcinomas.
MELK promotes cell migration and invasion via the FAK (show PTK2 ELISA Kits)/Paxillin (show PXN ELISA Kits) pathway, and plays an important role in the occurrence and development of gastric cancer.
Phosphorylation of the activation loop of MPK38 induces its movement resulting in kinase activation.
These results indicate that Trx (show TXN ELISA Kits) functions as a physiological inhibitor of MPK38, which plays an important role in inducing ASK1 (show MAP3K5 ELISA Kits)-, TGF-beta (show TGFB1 ELISA Kits), and p53 (show TP53 ELISA Kits)-mediated activity
an important role for MPK38-mediated phosphorylation of PDK1 (show PDPK1 ELISA Kits) in the negative regulation of PDK1 (show PDPK1 ELISA Kits) activity.
MPK38 may act as a novel regulator for promoting p53 (show TP53 ELISA Kits) activity through direct phosphorylation of p53 (show TP53 ELISA Kits) at Ser (show SIGLEC1 ELISA Kits)(15).
Upregulation of maternal embryonic leucine zipper kinase is associated with mammary tumor.
MELK is necessary for proliferation of embryonic and postnatal MNP and suggest that it regulates the transition from GFAP (show GFAP ELISA Kits)-expressing progenitors to rapid amplifying progenitors in the postnatal brain.
The characterization of two novel E2F (show E2F1 ELISA Kits) target genes, chromosome condensation-related SMC-associated protein 1 (Cnap1) and maternal embryonic leucine zipper kinase (Melk) is reported.
MPK38 physically interacts with ASK1 (show MAP3K5 ELISA Kits) in vivo and acts as a positive upstream regulator of ASK1 (show MAP3K5 ELISA Kits)
Melk-like gene may play a role in primitive hematopoiesis by affecting the expression of genes critical for hematopoiesis.
Overexpression of xMELK leads to failure of cytokinesis and impairs accumulation RhoA- a pivotal regulator of cytokinesis.
These results demonstrate the presence of a mitochondrial targeting signal at the N-terminus of the MC domain of MELK. This mitochondrial targeting signal was also functional in human HeLa cells.[MELK]
Serine/threonine-protein kinase involved in various processes such as cell cycle regulation, self-renewal of stem cells, apoptosis and splicing regulation (By similarity). Also plays a role in primitive hematopoiesis, possibly by affecting the expression of genes critical for hematopoiesis.
maternal embryonic leucine zipper kinase
, maternal embryonic leucine zipper kinase-like
, pEg3 kinase
, protein kinase Eg3
, protein kinase PK38
, tyrosine-protein kinase MELK
, Protein kinase Eg3