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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

KIAA1804 mixed lineage kinase 4

MLK4, KIAA1804
Top mentioned proteins: p38, ERK, beta Catenin, AP-1, MLK3
Papers on MLK4
Recurrent MLK4 Loss-of-Function Mutations Suppress JNK Signaling to Promote Colon Tumorigenesis.
Brognard et al., Manchester, United Kingdom. In Cancer Res, Jan 2016
UNASSIGNED: MLK4 is a member of the mixed-lineage family of kinases that regulate the JNK, p38, and ERK kinase signaling pathways.
DNA methylation changes in genes frequently mutated in sporadic colorectal cancer and in the DNA repair and Wnt/β-catenin signaling pathway genes.
Nilsson et al., Örebro, Sweden. In Epigenomics, 2014
RESULTS: We found significantly aberrant methylation in 23 genes (NEIL1, NEIL3, DCLRE1C, NHEJ1, GTF2H5, CCNH, CTNNB1, DKK2, DKK3, FZD5 LRP5, TLE3, WNT2, WNT3A, WNT6, TCF7L1, CASP8, EDNRB1, GPC6, KIAA1804, MYO1B, SMAD2 and TTN).
Mixed lineage kinase MLK4 is activated in colorectal cancers where it synergistically cooperates with activated RAS signaling in driving tumorigenesis.
Bardelli et al., Torino, Italy. In Cancer Res, 2013
Comprehensive mutational analyses have revealed that the mixed lineage kinase 4 (MLK4) protein kinase is frequently mutated in MSS CRC with approximately 50% of the mutations occurring in KRAS- or BRAF-mutant tumors.
MLK4 has negative effect on TLR4 signaling.
Han et al., Xiamen, China. In Cell Mol Immunol, 2012
MLK4 is a negative regulator of TLR4 signaling.
MLK4β functions as a negative regulator of MAPK signaling and cell invasion.
Chadee et al., Toledo, United States. In Oncogenesis, 2011
Mixed lineage kinase (MLK) 4, or MLK4, is a member of the MLK family of mitogen-activated protein kinase kinase kinases (MAP3Ks).
Cloning and Initial Functional Characterization of Mlk4α and Mlk4β.
Zabarovsky et al., Stockholm, Sweden. In Genomics Insights, 2010
We have cloned a novel human mixed-lineage kinase gene, MLK4.
Genomic profiling of 766 cancer-related genes in archived esophageal normal and carcinoma tissues.
Fan et al., San Diego, United States. In Int J Cancer, 2008
We also detected significant differences in germline allele frequency between the esophageal cohort of our study and normal control samples from the International HapMap Project for 10 genes (CSF1, KIAA1804, IL2, PMS2, IRF7, FLT3, NTRK2, MAP3K9, ERBB2 and PRKAR1A), suggesting that they might play roles in esophageal cancer susceptibility and/or development.
Absence of tyrosine kinase mutations in Japanese colorectal cancer patients.
Omata et al., Tokyo, Japan. In Oncogene, 2007
To further explore these mutations, we examined all reported mutations of NTRK3, FES, KDR, EPHA3, NTRK2, JAK1, PDGFRA, EPHA7, EPHA8, ERBB4, FGFR1, MLK4 and GUCY2F genes in the 24 colorectal cancer cell lines.
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