Ask about this productRelated genes to: MELK antibody
- Gene:
- MELK NIH gene
- Name:
- maternal embryonic leucine zipper kinase
- Previous symbol:
- -
- Synonyms:
- KIAA0175
- Chromosome:
- 9p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-04
- Date modifiied:
- 2016-10-05
Related products to: MELK antibody
Related articles to: MELK antibody
- There is a lack of robust evidence regarding immunosuppressive therapy in children and adolescents after kidney transplantation (KTx), and as such, international practice is highly variable. Recent clinical practice recommendations advocating individualized immunosuppressive strategies that incorporate newer agents are often not implemented. This can potentially contribute to reduced patient and renal allograft survival. - Source: PubMed
Publication date: 2026/06/18
Grünewald AnnaAhlenstiel-Grunow ThuridArslan ZainabBattelino NinaRachisan Andreea-Liana BotBouts AntoniaBusutti MarcoCornelissen Elisabethde Jong HuibDudley JanDüzova AliEibensteiner FabianFichtner AlexanderFomina SvitlanaGonzalez Mercedes LopezGulhan BoraGrabitz CarlHogan JulienHöcker BrittaJeruschke StefanieKanzelmeyer NeleKim Jon JimKorst UweLabbadia RaffaelaLitwin MieczysławMarks StephenMelk AnetteNovljan GregorObrycki LukaszOh JunPape NilsPasini AndreaPatry ChristianPohl MartinPreka EvgeniaPrytula AgnieszkaRieger SusanneSchiffer MarioSchild RaphaelSeeman TomasStojanovic JelenaTesta SaraTönshoff BurkhardTorres Diletta DomenicaWeber Lutz TNothacker MonikaPape Lars - Fungal infections contribute substantially to morbidity and mortality after kidney transplantation, yet pathogen-specific epidemiology and clinical risk profiles remain incompletely defined. We aimed to characterize incidence, timing, and pathogen-specific risk factors in a contemporary multicenter cohort. - Source: PubMed
Publication date: 2026/06/08
Schröter IrisSchindler DanielaMorath ChristianRenders LutzAndrassy JoachimKanzelmeyer NeleSchork AnjaZeier MartinGiese ThomasSommerer Claudia - With a wide range of genetic characteristics and metabolic requirements, diffuse large B-cell lymphoma (DLBCL) is an extremely complex cancer. Although maternal embryonic leucine zipper kinase (MELK) has been linked to the development of tumors, its function in DLBCL and control of cuproptosis, a copper-dependent mechanism of cell deathproduce, is yet unknown. Hub genes in DLBCL were found using integrated bioinformatic analysis of the TCGA and GEO datasets. Using qRT-PCR, WB, cell viability, Transwell, and mitochondrial assays, MELK expression was examined in DLBCL cell lines (OCI-LY8, U2932, OCI-LY7) and normal B cells (GM12878). Functional analyses were conducted in selected DLBCL cell lines (OCI-LY7 and OCI-LY8) to accurately assess the biological roles of MELK. Elesclomol (15 nM) and copper chloride (CuCl₂, 10 µM) were used to induce cuproptosis, while DLAT overexpression and S6 kinase inhibition were used to clarify signaling processes. MELK expression was considerably elevated in DLBCL tissues and cell lines (P < 0.05). In addition to inducing mitochondrial malfunction, increasing reactive oxygen species, lowering the NADH/NAD⁺ ratio, and triggering intrinsic apoptosis, MELK silencing inhibited proliferation, migration, and invasion. MELK knockdown enhanced the sensitivity of cells to elesclomol-Cu treatment, which in turn induced cuproptosis and further reduced MELK expression. Mechanistically, MELK overexpression increased cell survival, elevated dihydrolipoamide S-acetyltransferase (DLAT), and triggered the PI3K/mTOR/S6K signaling pathway. On the other hand, MELK-mediated effects on cuproptosis and intracellular copper buildup were abolished by S6K suppression or DLAT overexpression. Through the PI3K/mTOR/S6K-DLAT axis, MELK imparts resistance to cuproptosis and increases DLBCL cell survival. MELK targeting may increase copper-induced cytotoxicity, offering a possible DLBCL treatment approach. - Source: PubMed
Publication date: 2026/06/02
Wang XiaoxiaoWang ChenchenWang ChenLi ManmanYe WeihuaShi MeinengHou YunhuaDing Ming - Ovarian cancer (OVCA) remains the most lethal gynecologic malignancy, with poor prognosis largely due to late-stage diagnosis and therapy resistance. Pyroptosis, a pro-inflammatory form of programmed cell death, has recently emerged as a regulator of tumor progression and immune regulation. This study aimed to systematically profile pyroptosis-related genes and identify robust biomarkers for OVCA. Microarray data from the GSE54388 dataset were analyzed to characterize pyroptosis-related gene expression. Immune cell infiltration was assessed using xCell, and pathway enrichment was performed via Gene Set Enrichment Analysis (GSEA). Weighted Gene Co-expression Network Analysis (WGCNA) identified hub genes, followed by Gene Ontology (GO) and Reactome enrichment. Machine learning algorithms (Support Vector Machine, XGBoost, and Generalized Linear Model) were employed for feature selection and biomarker identification. Validation was conducted across independent bulk and scRNA-seq datasets, with GEPIA2 used to compare OVCA and normal samples and KMplot for survival analysis. OVCA samples showed significantly reduced infiltration of CD4 and CD8 T cells, mast cells, monocytes, neutrophils, and immature dendritic cells compared to normal samples. GSEA revealed enrichment of cell cycle-related pathways, implicating pyroptosis-related genes as key regulators of mitotic progression. From 1097 differentially expressed genes, 22 pyroptosis-related DEGs (PYRDEGs) were identified, with nine hub genes (CASP1, CEP55, CHMP4C, HTRA1, IL18, MELK, PKM, PTX3, TNFSF13B) strongly associated with OVCA. Functional enrichment linked these genes to cytokinesis, inflammasome activity, and immune signaling. Machine learning consistently identified CEP55 as the core biomarker, demonstrating high diagnostic accuracy (AUC up to 0.972) and significant upregulation in OVCA samples. Correlation analysis linked CEP55 expression to altered immune cell populations, including positive associations with Th1 and class-switched memory B-cells and negative associations with iDCs, Tregs, and M2 macrophages. CEP55 was highly expressed across bulk and scRNA-seq datasets (cancer epithelial and CD8+ TEMRA cells) and negatively correlated with overall survival (OS) and progression-free survival (PFS). Pyroptosis-related genes play pivotal roles in OVCA pathogenesis. CEP55 emerges as a promising biomarker for early detection and a potential therapeutic target, bridging cell cycle regulation with immune modulation. - Source: PubMed
Publication date: 2026/05/21
Arya RakeshBiswas Viplov KumarShakya HemlataKim Jong-Joo - Cervical cancer (CC) ranks as the fourth most prevalent cancer in women worldwide. While biomarkers exist, previous studies are often limited by public dataset heterogeneity, incomplete spectrum coverage, or lack of clinical validation. To address these limitations, this study aims to profile fresh tissues spanning the full continuum to systematically identify hub genes with dysregulated expression during malignant progression. - Source: PubMed
Publication date: 2026/05/20
Li PengShao YawenWang JunlingLin Ru