Ask about this productRelated genes to: TNIK antibody
- Gene:
- TNIK NIH gene
- Name:
- TRAF2 and NCK interacting kinase
- Previous symbol:
- -
- Synonyms:
- KIAA0551
- Chromosome:
- 3q26.2-q26.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2018-11-19
Related products to: TNIK antibody
Related articles to: TNIK antibody
- The organ- and stage-specific diversity of megakaryocytes (MKs) has prompted a reassessment of their distribution and functions. By integrating single-cell transcriptomic data across multiple organs and developmental stages, we identified previously unreported MK and platelet markers, including Tnik, a key regulator of MK function and platelet production. Using these markers alongside established ones, we developed a machine learning-based MK identification system (MKIDS) that enables MK detection in the brain, heart, and placenta in mice and humans. Functional studies demonstrated that brain-resident MKs are essential for neural development, underscoring organ-specific roles of MKs in regulating tissue development and function. Transcriptomic integration of MKs across organs and stages, with functional validation, revealed a developmental shift in platelet production-from a mitochondria-low to a mitochondria-enriched subpopulation. Our findings offer a transformative perspective on the MK system, highlighting its cellular diversity, functional complexity, and developmental dynamics. - Source: PubMed
Publication date: 2026/05/11
Xia MeijuanMa YeziCai YifeiZhao JingjingZhong YaoGuo SibeiLi MinminSu PeiShen BiaoHe HuizhenChen XiaoyuanZheng LinLi LeHuo ZiqiZhou WenWang FeiLiu CuicuiWang HongtaoZhou Jiaxi - Medulloblastoma (MB) is the most common malignant pediatric brain tumor and comprises molecularly and clinically distinct subgroups with highly variable outcomes. While survival rates exceed 80% in some subgroups, others remain associated with substantially poorer prognosis and increased risk of relapse. Current treatment includes surgery, radiation, and chemotherapy, which can result in significant long-term treatment-related morbidity. These challenges highlight the need to identify novel biomarkers and potential therapeutic targets to improve risk stratification and enable more tailored treatment approaches. The Traf2- and Nck-interacting kinase (TNIK) is a regulator of Wnt/β-catenin signaling and has been implicated in the progression of several cancers, but its role in MB remains unclear. - Source: PubMed
Publication date: 2026/05/08
Klaus Franz-LeonardMaragkou TheoniDelbridge ClaireEberhardt Charles GHewer EkkehardGocke AntoniaRadpour RaminMawrin ChristianMogler CarolinNeumann Julia EForster Stefan - Chemotherapy-induced peripheral neuropathy (CIPN) is a major dose-limiting side effect of cancer treatment, yet the lack of predictive human models continues to hinder therapeutic progress. Here, we establish a scalable and reproducible model of paclitaxel-induced axon degeneration and neurotoxicity in human iPSC-derived sensory neurons, suitable for high-throughput identification of neuroprotective compounds. Using this platform, we screen a library of 192 kinase inhibitors and identify 19 hits that commonly inhibit three STE20 kinases-MAP4K4, MINK1, and TNIK. Genetic knockdown studies reveal that multi-kinase inhibition of these kinases is required for neuroprotection against paclitaxel. Consistently, selective pharmacological inhibition of the identified STE20 kinases rescues paclitaxel-induced axon degeneration in iPSC-derived sensory neurons and primary human dorsal root ganglia (DRG) and preserves intraepidermal nerve fiber density in a mouse model of CIPN. Together, these findings establish a translational human sensory neuron platform that enables target validation and drug discovery for CIPN. - Source: PubMed
Publication date: 2026/05/06
Petrova VeselinaMills Caitlin EHug ClemensCetinkaya-Fisgin AyselSplaine JenniferFouladzadeh SepidehHakim SaraPowell RasheenZhen ShannonChung MirraBradshaw Gary ADeng TaoSingec IlyasWang QingKawaguchi RikiJonnagaddala HarathiBarrett Lee BSmith Jennifer AKalocsay MarianGyori Benjamin MHoke AhmetSorger Peter KWoolf Clifford J - Human induced pluripotent stem cell (iPSC)-derived neurons provide a platform for modeling brain disorders. Among disease-relevant cellular phenotypes, impaired neurite outgrowth has emerged as an indicator reflecting key aspects of neurological disease pathophysiology. We conducted a high-throughput phenotypic screening of over 21,000 small molecules to identify compounds that enhance neurite outgrowth in iPSC-derived neurons, and we identified three bioactive compounds sharing a common indazole scaffold. Notably, one of these compounds selectively targets TNIK, a kinase involved in neuronal development. Scaffold expansion led to the discovery of thienopyridone derivatives with potent neurite-promoting activity. Two thienopyridone compounds were further validated in a human neural organoid model, in which their neurite outgrowth-promoting effects were reproducibly confirmed. Transcriptomic profiling revealed activation of signaling pathways associated with neurotrophic stimulation. These findings identify thienopyridones as a scaffold for neuritogenic small molecules, suggesting their potential as a therapeutic strategy for brain disorders and for promoting neural regeneration. - Source: PubMed
Publication date: 2026/03/30
Imamura KeikoYukikate HiroshiHioki TakeshiOkusa AyaShibata KeisukeNarvaiza IñigoKaieda AkiraSaito BunnaiSakai NozomuAnh Suong Dang NgocNiki TakeshiArioka YukoOzaki NorioInoue Haruhisa - Drug discovery has been constrained by extended timelines and high costs, as the cumulative requirements of preclinical validation, multi-phase clinical trials, and regulatory approval have been imposed. Recently, computational modeling has been explored as a supportive approach to accelerate the identification and refinement of therapeutic candidates. Proof-of-concept was provided in a phase 2a trial of a de novo-designed TNIK inhibitor in idiopathic pulmonary fibrosis, in which safety, tolerability, and pharmacodynamic target engagement were demonstrated, with a trend toward reduced functional decline. This study showed that AI-derived molecules can advance into human testing, but broader validation, mechanistic understanding, and regulatory alignment remain essential. In oncology, where tumor heterogeneity, clonal evolution, and therapeutic resistance continue to constrain durable clinical benefit, there is an increasing need for adaptive and data-informed drug discovery strategies. This Perspective reviews recent progress and limitations in AI-driven drug discovery and early clinical translation. It emphasizes how the clinical evaluation of an AI-generated TNIK inhibitor serves as an early translational reference and outlines practical strategies for integrating multi-omics data, federated model validation, and adaptive trial design to advance precision oncology-oriented therapeutics. - Source: PubMed
Publication date: 2026/04/15
Yoo Wonbeak