MEK5
- Known as:
- MEK5
- Catalog number:
- 000099A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MEK5
Related genes to: MEK5
- Gene:
- MAP2K5 NIH gene
- Name:
- mitogen-activated protein kinase kinase 5
- Previous symbol:
- PRKMK5
- Synonyms:
- MEK5, MAPKK5, HsT17454
- Chromosome:
- 15q23
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-11
- Date modifiied:
- 2016-10-05
Related products to: MEK5
Related articles to: MEK5
- Numerous genetic variants have been identified by genome-wide association studies as being associated with colorectal cancer (CRC) risk. Metabolome-wide association analysis was performed for 187 CRC-associated genetic variants using genomic data and untargeted H nuclear magnetic resonance urine metabolomics from 1951 Airwave Health Monitoring Study participants. We identified statistically significant associations between seven CRC single-nucleotide polymorphisms (SNPs) and urinary metabolites. This included SNPs within or close to with sucrose ( = 1.2 × 10), with amino acids ( = 6.9 × 10 with tyrosine, = 9.9 × 10 with leucine), and and with gut microbial metabolites ( = 1.6 × 10 and = 4.4 × 10). The most significant correlation was followed by functional experiments in Caco-2 colon cancer cells. CRISPR-mediated knockout of a 48-nt intronic region containing rs10411210 in colon cancer cells compromised cell growth. RNA sequencing was performed in the two sets of clones (3 edited and 3 unedited) followed by pathway enrichment, and gene ontology analysis depicted extensive deregulation of genes (448 up- and 195 downregulated) involved in cell division and several metabolic processes. Overall, these findings demonstrate that integrating genetic and metabolomic data highlights the importance of the intronic locus in CRC potentially through metabolic processes affecting excretion of dietary and other metabolites. - Source: PubMed
Publication date: 2026/01/28
Iliou AikateriniChekmeneva ElenaPinto Rui ClimacoKoukouzeli Fotini ENtounias YiannisGeorgakopoulou KonstantinaPouliou MarialenaAgelopoulos MariosTsilidis Konstantinos KGunter Marc JElliott PaulGriffin Julian LDehghan AbbasKlinakis ApostolosMikros EmmanuelTzoulaki Ioanna - Perfluorooctanesulfonic acid (PFOS) is a persistent environmental pollutant widely present in ecosystems and humans, linked to numerous diseases, including cancers, due to its potent toxicity. Despite its harmful effects, effective strategies for mitigating PFOS-induced toxicity remain undeveloped or at best underdeveloped. In this effort, we explore the concept of toxicity reversal by loci-specific DNA methylation editing to reverse PFOS-induced toxicity, whereby key cellular processes such as proliferation, migration, and apoptosis are restored. To demonstrate our concept, we employed CRISPR-dCas9 epigenome editing tools, utilizing catalytically deactivated Cas9 fused with either DNA methyltransferases or ten-eleven translocation () dioxygenase effectors for loci-specific epigenome editing. Gene expression changes related to kidney disease, metabolism, and DNA methylation pathways were first noted. Through reduced representation bisulfite sequencing (RRBS), we demonstrated how PFOS exposure disrupts the epigenetic landscape, altering transcription factor binding sites linked to tumorigenesis, inflammation, and stress. By methylation editing of a single CpG site in implicated genes such as and , we effectively reversed PFAS-induced toxicity and restored essential cell functions. Our success in precise single-CpG methylation editing of target genes effectively reverses toxicity, marking the first application of epigenome editing tools to counteract the toxic effects of a persistent environmental contaminant (PFAS). Our approach offers promising potential for toxicological screening and the identification of therapeutic targets to mitigate adverse effects triggered by environmental toxicants. - Source: PubMed
Publication date: 2025/08/21
Sands MiaWen YiSachdeva ArshveerIrudayaraj Joseph - With increasing life expectancy, the prevalence of cardiovascular disease (CVD) accompanied by comorbidities is rising, presenting a growing challenge for healthcare systems. Understanding shared genetic factors underlying CVD and its comorbid conditions may facilitate the development of more effective strategies for prevention and treatment. - Source: PubMed
Publication date: 2025/11/26
Mishra Binisha HMishra Pashupati P - Liver hepatocellular carcinoma (LIHC) is a common cancer worldwide. Mitogen-activated protein kinase kinase (MAP2Ks) are related to the occurrence and development of a variety of tumors. However, the expression pattern, role, and prognostic value of the 7 MAP2K family members in LIHC have not yet been elucidated. We used the Oncomine, UALCAN, Human Protein Atlas, GeneMANIA, Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, TIMER, and Kaplan-Meier Plotter databases. On August 7, 2021, we searched these databases for the terms MAP2K1, MAP2K2, MAP2K3, MAP2K4, MAP2K5, MAP2K6, MAP2K7, and "liver cancer." The exposure group comprised LIHC patients, and the control group comprised normal patients (those with noncancerous liver tissue). All patients shown in the retrieval language search were included. We compared the mRNA expression of these proteins in LIHC and control patients to examine the potential role of MAP2K1 to 7 in LIHC. Relative to the normal liver tissue, mRNA expression of MAP2K1/3 was significantly downregulated (P < .001), MAP2K4 was downregulated (P < .05), and that of MAP2K2/5/6/7 significantly upregulated (P < .001), in LIHC. MAP2K mRNA expression varied with gender (P < .0001), cancer stage (P < .05), tumor grade (P < .05), and with node metastasis status (P < .05), except for MAP2K4. Based on Kyoto Encyclopedia of Genes and Genomes enrichment analysis, these genes were associated with the following pathways: MAPK signaling pathway, GnRH signaling pathway, Fc epsilon RI signaling pathway (P < .05). The MAP2Ks were significantly associated with purity (P < .05), except for MAP2K1/2, with B cell (P < .05), except for MAP2K3, and that all significantly associated withCD8+ T cell, CD4+ T cell, macrophage, neutrophil, and dendritic cell infiltration (P < .05). High mRNA expression of MAP2K1/3/4/5 (P < .05) and low expression of MAP2K6 (P < .05) indicated overall survival, the high expression of MAP2K3/4/5 were related to relapse free survival and progression free survival; the high expression of MAP2K3/5/7 were related to disease free survival. We identified MAP2K1 to 7 as potential diagnostic markers, and MAP2K2 to 7 as prognostic markers, of LIHC. Our future work will promote the use of MAP2Ks in the diagnosis and treatment of LIHC. - Source: PubMed
Dong ShenJing ShenQinshun JiaoHuaning WangRong Zhu - Imprinted genes are epigenetically regulated in normal tissues to follow monoallelic expression according to the parent of origin of each allele. Some of these patterns are dysregulated in cancer. - Source: PubMed
Publication date: 2025/05/25
Krushkal JuliaJensen Travis LWright GeorgeZhao Yingdong