Ask about this productRelated genes to: MAP3K15 antibody
- Gene:
- MAP3K15 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase 15
- Previous symbol:
- -
- Synonyms:
- bA723P2.3, FLJ16518, ASK3
- Chromosome:
- Xp22.12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-24
- Date modifiied:
- 2015-09-03
Related products to: MAP3K15 antibody
Related articles to: MAP3K15 antibody
- Tandem repeat expansions (TREs) cause over 60 known neurological, neuromuscular, and developmental disorders. Detecting these expansions genome-wide is challenging due to their size, sequence complexity (including interruptions), and population variation. While long-read sequencing is an emerging technology that can fully resolve many TREs, no methods have been described for genome-wide identification and prioritization of candidate pathogenic TREs with this technology. - Source: PubMed
Publication date: 2026/05/01
Gibson Sophia BDamaraju NikhitaGustafson J GusBalton Elsa VChanprasert SirisakGlass Ian AHorike-Pyne MarthaKumar Runjun DLeppig Kathleen ALundberg ChrisRanchalis JaneRosenthal Elisabeth ASolomon Andrew KStergachis Andrew BWener Mark Jarvik Gail PBlue Elizabeth EDipple Katrina MDashnow HarrietStarita Lea MMiller Danny E - Sphingosine-1-phosphate receptor 1 (S1PR1) signaling has been linked to the regulation of immunosuppressive cell populations within the tumor microenvironment (TME); however, its role in shaping anti-tumor CD8⁺ T cell responses remains poorly defined. Herein, we demonstrate that intratumoral CD8⁺ T cells express S1PR1, with expression predominantly enriched in the terminally exhausted subset. Transcriptomic profiling, combined with pharmacological inhibition and genetic knockdown, reveals that S1PR1-S1P signaling activates the PERK (protein kinase R (PKR)-like endoplasmic reticulum kinase)-CHOP (C/EBP homologous protein) axis of the endoplasmic reticulum stress response. CHOP, in turn, upregulates transcription of Map3k13 and Map3k15, triggering downstream MAPK signaling and culminating in activation of p38MAPK. Activation of this pathway impairs CD8⁺ T cell metabolism and effector function while increasing apoptotic susceptibility. This ultimately limits the persistence and accumulation of functional CD8⁺ T cells within the TME, thereby compromising their responsiveness to anti-PD-1 therapy. Targeting the S1PR1-S1P axis or its downstream effectors offers a promising strategy to improve cancer immunotherapy outcomes. - Source: PubMed
Publication date: 2026/03/19
Basak DebashreeGhosh PuspenduGautam AnupamSarkar IshitaBhoumik ArpitaChowdhury SohamMahanti ShaunMandal AnweshaChakraborty RajeswariKar AnweshaChowdhury SnehanshuKumar KrishnaBarman ShubhrajitGanesan Senthil KumarChakrabarti SaikatPaul SandipChatterjee Shilpak - The mitogen-activated protein kinase (MAPK) pathway is a conserved signaling system that responds to extracellular signals and translates them into appropriate cellular responses. While multiple MAPK kinase kinases (MAP3Ks) play a crucial role in the step wise transmission of MAPK signals in response to the pathogen infection, little is known about the function of MAP3K15 (also known as apoptosis signal-regulated kinase 3, ASK3) in viral infection. Here, we provide evidence that shrimp MAP3K15 undergoes phosphorylation and activation during a DNA virus, white spot syndrome virus (WSSV) infection, the activated MAP3K15 interacted with the NF-кB homolog, Dorsal, to promote its nuclear translocation for expression of the coiled-coil-containing C-type lectin (CC-CL) and the viral immediate early (ie) genes. CC-CL then activates the JAK/STAT pathway as the ligand to its membrane receptor Domeless, driving the expression of more ie genes. In addition, the JNK/P38 signaling pathway is also activated to promote viral ie genes expression. Importantly, the viral amplification in a wide range of crustaceans were inhibited and the survival rates of host were improved effectively by suppressing MAP3K15 expression or utilizing SDK1, an inhibitor targeting the active form of MAP3K15, suggesting that the MAP3K15 has a critical and conserved function in viral infection. Taken together, this study elucidates a pivotal role and mechanism of MAP3K15 in DNA virus infection, providing novel insights and potential strategies for the control of WSSV infection in crustaceans aquaculture practice. - Source: PubMed
Publication date: 2025/08/01
Ran Xiao-QinLiu Chen-ChenXu Xue-MeiWu Xin-MengKang Cui-Jie - Congenital heart disease (CHD) exhibits a marked male predominance in birth prevalence, yet the genetic mechanisms underlying this sex disparity remain poorly understood. This study investigates the contribution of rare damaging variants on autosomes and the X chromosome to sex differences in foetal CHD. - Source: PubMed
Publication date: 2025/05/09
Sun HairuiHao XiaoyanLiu HankuiZhang SiyaoHan JianchengZhang YeLiu TingtingYang XianWang HairuiFan JiaqiGuan YuxuanPeng NiXie JiaoyangXia HongmeiJi XueqinXu YanZhang JianguoWang JianbinLan FengZhang HongjiaGu XiaoyanHe Yihua - Idiopathic pulmonary fibrosis (IPF) is a progressive lung disorder that is characterized by the disruption of lung architecture and respiratory failure. Notwithstanding the advent of novel therapeutic agents such as pirfenidone and nintedanib, there remains a pressing need for the development of innovative diagnostic and therapeutic strategies. Next-generation sequencing allows for the analysis of gene expression and the discovery of biomarkers. The objective of our study was to identify IPF-specific gene signatures, construct a diagnostic nomogram, and explore the role of the extracellular matrix (ECM) and epithelial-to-mesenchymal transition (EMT) in IPF pathogenesis. Utilizing data from the Gene Expression Omnibus (GEO) database, we identified differentially expressed genes (DEGs), performed weighted correlation network analysis (WGCNA), and constructed a nomogram. The present study has identified a group of key genes that are associated with IPF. The identified genes include GREM1, ITLN2, MAP3K15, RGS9BP, and SLCO1A2. The results of the immunohistochemical analysis indicated a significant correlation between these central genes and immune cell infiltration. Furthermore, Gene Set Enrichment Analysis (GSEA) revealed that these genes play a critical role in the pathogenesis of IPF. To validate the diagnostic potential of these core genes, we performed confirmatory analyses in independent Gene Expression Omnibus (GEO) datasets. We observed a significant upregulation of GREM1 expression in IPF animal and cellular models. These findings provide new insights into the molecular mechanisms of IPF and suggest potential targets for future diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2025/04/03
Huang XiangfeiYu WenTian JuanZhang YangWei AipingLi YongChen Shibiao