Ask about this productRelated genes to: TPX2 antibody
- Gene:
- TPX2 NIH gene
- Name:
- TPX2 microtubule nucleation factor
- Previous symbol:
- C20orf2, C20orf1
- Synonyms:
- p100, DIL-2
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-29
- Date modifiied:
- 2019-01-21
Related products to: TPX2 antibody
Related articles to: TPX2 antibody
- Animal cells assemble gigadalton-scale molecular complexes composed of ~200 proteins to build a functional centrosome during mitosis, ensuring faithful chromosome segregation. Although the molecular principles underlying centrosome assembly have been extensively studied, the minimal components required to reconstitute centrosome-like activity in living cells remain unknown. Here, we develop an optogenetic strategy that exploits Aurora A kinase clustering to assemble functional centrosome-like structures in human cells. Remarkably, these light-induced assemblies activate Aurora A, nucleate microtubules, and bypass the requirement for the canonical Aurora A scaffold Cep192. Mechanistically, we identify the evolutionarily conserved Aurora A partner TPX2 as an essential factor for Aurora A cluster-dependent microtubule nucleation. Furthermore, optogenetic Aurora A clustering significantly rescues spindle assembly defects associated with centrosome ablation. We term this approach Light-Induced Spindle Assembly (LISA). By directly coupling Aurora A activity to spatial clustering, LISA defines a minimal and tunable module capable of driving spindle assembly. More broadly, LISA provides a synthetic biology platform for dissecting the fundamental principles of Aurora A-dependent spindle assembly, a prominent feature of mitotic and meiotic spindle formation. - Source: PubMed
Publication date: 2026/09/15
Olakkal VigneshBalakrishnan MadhumithaKotak Sachin - Protein-protein interactions (PPIs) regulate essential cellular processes and represent an important class of therapeutic targets; however, discovering effective modulators of PPIs remains a formidable challenge. Although deep learning approaches have been widely explored for PPI modulator discovery, many rely on simplified representations that obscure interchain boundary information and fine-grained PPI-modulator interaction (PPIMI) patterns, limiting their robustness under distribution shifts. To address this challenge, we introduce TvTPPIMI, a framework that leverages learnable boundary tokens to encode partner-aware boundary information and models PPIMI at atom-residue resolution. In a case study targeting the AURKA-TPX2 interaction, TvTPPIMI prioritized putative modulatory candidates from a small-molecule screening library. Structure-based docking, attention analysis, multireplica molecular dynamics simulations, MM/GBSA binding free-energy estimation, and noncovalent interaction analyses provided post hoc physical support for the stable AURKA binding of selected candidates, highlighting CE02-6266 as the most favorable compound among the tested hits. Together, these results suggest that TvTPPIMI provides a generalizable computational framework with coarse-grained, attention-based interpretive cues for PPIMI prediction and can be integrated with structure- and dynamics-based analyses to support PPI modulator discovery. - Source: PubMed
Yang LanChen JingTan HongLiu FuruiFang ZhongchengYuan YajingWang HanSun HeqiLi JiayiWei DongQing - Liposarcoma (LPS) is a common soft tissue sarcoma; however, its molecular pathogenesis and immune cell infiltration remain poorly understood. This study investigated potential driver genes and pathways in LPS and characterized immune cell infiltration patterns to identify potential markers for targeted therapy. Differentially expressed genes (DEGs) in LPS were analyzed by GO and KEGG pathway enrichment analysis. A protein-protein interaction network was constructed using the STRING database and visualized with Cytoscape. mRNA expression of genes with high |logFC| values was verified by RT-qPCR. Immune cell subsets were quantified using CIBERSORT. GO and KEGG analysis revealed significant functional clusters and pathways, and most verified genes were consistent with the bioinformatics analysis. Survival analysis showed that high expression of TYMS, KIF20A, BUB1B, LMNB1, RRM2, ZWINT, and RACGAP1 was significantly associated with poor overall survival and poor disease-free survival (DFS). High levels of TMSB15A, TPX2, PKM2, and PTTG1 were significantly associated with poor DFS alone. CIBERSORT analysis identified a significantly higher fraction of resting mast cells (MCs) in LPS tissues compared to normal fatty tissues (P < 0.05). TOP2A, IL-6, PCNA, CDK1, JUN, MYC, CCNB1, EGFR, ACACB, and BIRC5 were identified as potential diagnostic biomarkers of LPS, providing strong evidence for hub gene studies. Immune cell infiltration analysis further suggested that resting MCs may play a potential role in LPS development, although further experimental validation is warranted. Collectively, these findings clarify the molecular basis of LPS and provide a foundation for future research into its treatment. - Source: PubMed
Publication date: 2026/09/11
Liu ChunxiaoWang YanhuaLiu QiuxiaZhang Sha - The hyperproliferation and aberrant inflammatory activation of epidermal keratinocytes constitute the core pathological features of psoriasis. While non-coding RNAs have emerged as critical epigenetic regulators, their specific contributions to psoriatic pathogenesis remain incompletely understood. In this study, we investigated the pathological significance of a novel circular RNA, circLDLR, which was identified via high-throughput sequencing and validated to be significantly upregulated in clinical psoriatic lesional tissues compared to normal skin. In vitro, utilizing an M5 cytokine-induced HaCaT keratinocyte model to mimic the psoriatic inflammatory microenvironment, we observed a concordant upregulation of circLDLR. Functional evaluations revealed that the targeted knockdown of circLDLR effectively mitigated M5-induced cellular hyperproliferation, pathological migration, and the excessive secretion of pro-inflammatory cytokines (IL-6, IL-1β, and IL-8). Mechanistically, RNA immunoprecipitation and dual-luciferase reporter assays elucidated that cytoplasmic circLDLR functions as a competing endogenous RNA (ceRNA) by physically sponging miR-1294, thereby de-repressing the expression of its downstream target, TPX2. Crucially, the phenotypic protection conferred by circLDLR silencing was significantly reversed by either miR-1294 inhibition or TPX2 overexpression. Collectively, our findings identify the circLDLR/miR-1294/TPX2 axis as a novel molecular driver of keratinocyte dysfunction, providing valuable histopathological insights and highlighting a promising therapeutic target for psoriasis. - Source: PubMed
Publication date: 2026/08/10
Tian JiangtianDeng XuanqiYin AnqiLiu WeiGao YugeLi YuzhenHao Siyu - - Source: PubMed
Publication date: 2026/08/10
Gu XiaoYao XiaocuiLiu Dengtao