Ask about this productRelated genes to: MAP4K4 antibody
- Gene:
- MAP4K4 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase kinase 4
- Previous symbol:
- -
- Synonyms:
- HGK, NIK, FLH21957
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2016-10-05
Related products to: MAP4K4 antibody
Related articles to: MAP4K4 antibody
- As the most common malignant renal tumor in children, the progression of Wilms' tumor is frequently driven by abnormal alternative splicing (AS), cell death imbalance, and an immunosuppressive microenvironment. However, the precise regulatory chain connecting these three critical elements remains largely unexplored. This study aimed to systematically construct and characterize an "AS-cell death-immunity" regulatory network in Wilms' tumor. - Source: PubMed
Publication date: 2026/08/06
Yang ChunleiLiao ManXu HaolunWang JunBao HaibinZhang ManLi CanZheng TianLi Gang - Doxorubicin (DOX) is a highly effective chemotherapeutic agent, but its clinical application was constrained by irreversible cardiotoxicity. Increasing evidence indicates that ferroptosis is a central mechanism of DOX-induced cardiotoxicity (DIC). Both the m⁶A demethylase FTO and yes-associated protein (YAP) are found to suppress ferroptosis in DIC. Importantly, both YAP and its upstream negative regulator, MAP4K4, are potential targets of FTO. However, whether FTO regulates DOX-induced cardiac ferroptosis via the MAP4K4/YAP signaling axis remains unexplored. - Source: PubMed
Publication date: 2026/07/07
Yan YouyouSong DandanLi LongboWang Junnan - Antiphospholipid syndrome (APS) is a systemic autoimmune disorder driven by antiphospholipid antibodies (aPLs), primarily characterized by recurrent thrombosis and pregnancy morbidity. Transcriptomic analyses of other immune compartments have provided insights into APS pathogenesis. However, despite the central role of platelets in APS pathophysiology, their transcriptomic features remain largely unexplored. We therefore aimed to characterize the platelet transcriptomic landscape in APS and identify key immune-thrombotic pathways. RNA sequencing and bioinformatic analyses of platelets from 43 APS patients, 20 asymptomatic aPL carriers, and 20 healthy controls revealed distinct proinflammatory transcriptional reprogramming, consistent with platelets as active thrombo-inflammatory hubs. APS platelets exhibited marked activation of innate immune (Toll-like and NOD-like receptors) and neutrophil pathways, which may contribute to disease propagation through a functional platelet-neutrophil axis. A 15-gene classifier (e.g., , ) discriminated APS from controls with high accuracy (Area Under the Curve 0.901-0.948). The classifier also highlighted molecular differences between APS and asymptomatic aPL carriers relevant to disease progression. Network analysis suggested that anti-β2-glycoprotein I antibodies were associated with unique coagulation-immunity modules, while arterial and venous thrombosis displayed divergent cytoskeletal-energetic and lipid-signaling signatures, respectively. Together, these findings suggest that platelets in APS acquire a distinct proinflammatory phenotype and function as key immunothrombotic interfaces, supporting disease stratification and platelet-derived diagnostic strategies. - Source: PubMed
Publication date: 2026/06/16
Yang YaqingJiang HaiyueTang ZihanLiu HongleiCheng XiaobingSu YutongYe JunnaHu QiongyiSun YueMeng JianfenChi HuihuiZhou ZhuochaoJia JinchaoWang MengyanMa YuningShi HuiTeng JialinYang ChengdeLiu Tingting - Transient Receptor Potential Melastatin 7 (TRPM7) is a 'chanzyme' with dual functions, acting both as a channel for divalent ions and as a serine/threonine kinase. Overexpression of TRPM7 has been linked to the development of various diseases, particularly cancers, making it a promising molecular target. Despite its relevance in oncogenesis, the phospho-regulatory network of TRPM7 remains largely unexplored, with limited evidence on its upstream kinases, downstream substrates, and site-specific phospho-regulated functions. - Source: PubMed
Publication date: 2026/06/01
Palollathil AkhinaMahin AlthafGopalakrishnan Athira PerunellySambreena AlimathShivamurthy Prathik BasthikoppaRaju Rajesh - Wilms' tumor (WT) is one of the most common pediatric abdominal malignancies. The RNA-binding protein heterogeneous nuclear ribonucleoprotein D (hnRNPD) is related to cancer progression through regulating target mRNA stability. Nonetheless, its expression profile and value for WT are largely unexplored. Human renal proximal tubular epithelial cells (RPTEC) and WT cells (17.94, HFWT) were employed as experimental models for exploring hnRNPD's effect on WT progression. Subsequently, potential downstream targets of hnRNPD were identified through bioinformatics analysis. Functional validation was performed in vitro by modulating hnRNPD and its candidate targets via gene silencing and overexpression methods. Alterations in gene expression was analyzed through qRT-PCR as well as Western blot. Besides, CCK-8 was conducted to evaluate cell proliferation, whereas scratch and Transwell assays to determine cell migration alongside invasion separately. Additionally, critical epithelial-mesenchymal transition (EMT)-associated protein expression, namely E-cadherin, N-cadherin, alongside vimentin, was detected to assess regulatory impact of hnRNPD on the EMT process. hnRNPD mRNA and protein expression significantly elevated within 17.94 and HFWT cells than in RPTEC cells. Silencing of hnRNPD in 17.94 cells inhibited cell proliferation, migration, and invasion. Concurrently, N-cadherin and Vimentin protein levels declined, and E-cadherin protein level increased. Conversely, overexpression of hnRNPD in HFWT cells markedly enhanced their malignant phenotypes and promoted EMT. Bioinformatics analysis identified mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) as a potential downstream target of hnRNPD in WT. Mechanistically, hnRNPD overexpression extended the half-life of MAP4K4 mRNA, and a specific physical interaction between hnRNPD protein and MAP4K4 mRNA was observed. Functional rescue experiments further demonstrated that silencing MAP4K4 inhibited tumor malignant progression, while overexpression of MAP4K4 reversed the tumor-suppressive effects induced by hnRNPD silencing. hnRNPD may promote EMT in WT cells by stabilizing MAP4K4 mRNA, suggesting a critical role for the hnRNPD-MAP4K4 axis in driving tumor progression. - Source: PubMed
Publication date: 2026/06/03
Li GangLiao ManBao HaibinXu HaolunWang JunZhang ManLi CanZheng TianYang Chunlei