MEK5 Recombinant Adenovirus
- Known as:
- MEK5 Recombinant Adenovirus
- Catalog number:
- ADV-129
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- MEK5 Recombinant Adenovirus
Related genes to: MEK5 Recombinant Adenovirus
- 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 Recombinant Adenovirus
Related articles to: MEK5 Recombinant Adenovirus
- Lower educational attainment is associated with obesity and type 2 diabetes (T2D), but prospective evidence, external validation, mediator patterns, and genetic triangulation have rarely been integrated. - Source: PubMed
Publication date: 2026/06/26
Geng GuannanQiu ShizhengZhang ZhishuaiLiu XinruWang XinHu YangKuang HongyuZhang Jiahui - Chemotherapy resistance in acute myeloid leukemia (AML) remains a major clinical challenge. Integration of multiomic profiling and in vivo functional genomics revealed splicing dysregulation as a determinant of chemoresistance in AML. We uncovered a network involving the splicing regulator SRRM1 and the CLK1/4 and PAK1 kinase families as vulnerabilities in chemoresistant AML cells. Both kinase families are hyperactivated in chemoresistant cells, promoting SRRM1 phosphorylation and altering its scaffolding function. We also identified a relapse-associated variant, c.1429G>T p.(Ala→Ser), that confers chemotherapy resistance. Combined PAK1 and CLK1/4 inhibition recapitulated the splicing changes induced by loss, preferentially targeting chemoresistant AML and enhancing chemotherapy efficacy in cell lines, primary cells, and mouse models. Last, we pinpointed MAP2K5 as a critical downstream effector because missplicing of exons 17 and 18 of upon SRRM1 depletion sensitized cells to chemotherapy. Our findings highlight a therapeutic strategy to overcome AML relapse by targeting splicing dysregulation. - Source: PubMed
Publication date: 2026/07/08
Vaganay CamilleLing FrankKelly Lois MCharles JulietteMeslin Paul-ArthurPasquer HélèneKim RathanaPasset MarieDuchmann MatthieuPelissier-Menjaud LéaLecourt SéverineSu Angela HLatour EmmanuelleBassil Christopher FAlexe GabrielaFortin GaelNhat Duong HoCuleux CécileLegrand CarineFodil SofianeHuynh TonySaadallah KhansaRamos AzucenaLombard BérangèreLoew DamarysDelaney Christopher DLonchamp CatherineFontaine MorganePacchiardi KimKocijancic AnjaAziez LisaFenouille NinaSebert MarieAdès LionelRaffoux EmmanuelHemann Michael TClappier EmmanuelleBenajiba LinaStegmaier KimberlyWood Kris CItzykson RaphaëlForget AntoineLobry CamillePuissant Alexandre - Restless legs syndrome (RLS) is a common sensorimotor disorder with limited treatment options and incompletely understood pathophysiology. Genome-wide association studies have identified numerous risk loci, but translating these findings into causal genes and therapeutic targets remains challenging. We performed a proteome-wide association study (PWAS) integrating RLS genome-wide association study (GWAS) data from FinnGen with two brain pQTL datasets (ROSMAP and Banner). We validated the identified proteins using TWAS, SMR, and colocalization analyses using brain pQTL and eQTL datasets. To further investigate peripheral protein associations, we performed SMR using plasma pQTL data from the UK Biobank Pharma Proteomics Project (UKB-PPP). We also conducted a phenome-wide association study (PheWAS) to screen for potential off-target effects of the prioritized genes, followed by drug prediction using DSigDB and molecular docking. PWAS identified , along with and , as significantly associated with RLS. was identified by brain-based SMR ( = 0.0001), colocalization (PP.H4 = 0.96), TWAS ( = 0.048), and was confirmed by plasma-based SMR ( = 3.16 × 10) as the only protein associated with RLS. PheWAS analysis, without associations for 783 non-RLS phenotypes, confirmed the specificity of . Among 27 predicted -targeting compounds, Gambierol had the strongest binding affinity (-8.3 kcal/mol). This proteogenomic study identifies as a prioritized causal gene and promising drug target for RLS, combining brain and plasma data to provide new insights into pathogenesis and candidate drug development. - Source: PubMed
Publication date: 2026/05/15
Zhang LingyuJin QianqianDu RuochenLiang Yuxiang - Genes play a pivotal role in appetite regulation and energy homeostasis during a person's obesity. LEP (Leptin) and POMC (Proopiomelanocortin) are vital for appetite suppression and promoting satiety, while AgRP (Agouti-related peptide) and NPY (Neuropeptide Y) serve to stimulate appetite, creating a balanced interplay between hunger and satiety signals. GHRL (Ghrelin) further promotes hunger, emphasizing the complexity of these regulatory mechanisms. BDNF (Brain-derived neurotrophic factor) shows a dual role, impacting energy homeostasis not only in the brain but also in adipose tissue, thereby influencing lipid metabolism. PCSK1 (Proprotein Convertase Subtilisin/Kexin Type 1) is critical for the processing of neuropeptides that modulate energy balance. IGF2BP2 (Insulin-like Growth Factor 2 mRNA-Binding Protein 2) and MAP2K5 (Mitogen-Activated Protein Kinase 5) contribute to metabolic processes involved in fat accumulation and glucose regulation. Thus, emphasizing the significance of these mechanisms offers valuable insights that could lead to effective interventions for obesity prevention and management. - Source: PubMed
Kaur HarmandeepKaushik DeepikaRasane PrasadOz FatihProestos CharalamposKumar Mukul - 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