Ask about this productRelated genes to: TACC3 antibody
- Gene:
- TACC3 NIH gene
- Name:
- transforming acidic coiled-coil containing protein 3
- Previous symbol:
- -
- Synonyms:
- ERIC1
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-12
- Date modifiied:
- 2019-04-23
Related products to: TACC3 antibody
Related articles to: TACC3 antibody
- Comprehensive genomic profiling test (CGPT) using next-generation sequencing (NGS) plays a vital role in cancer diagnosis, treatment option, and prognostic evaluation. In Japan, three tissue-based CGPTs, FoundationOne® CDx, GenMineTOP, and NCC OncoGuide™, are reimbursed under public health insurance. However, their comparative performance in central nervous system (CNS) tumors remains unclear. - Source: PubMed
Publication date: 2026/05/06
Kawauchi DaisukeOhno MakotoTakahashi MasamichiKoyama TakafumiSunami KunikoHirata MakotoYanagisawa ShunsukeOmura TakakiAoki TakumaFujii GentaSaito KojiYamamoto TetsuyaSuzuki HiromichiNarita Yoshitaka - A wide spectrum of genomic events leading to dysregulated fibroblast growth factor receptor (FGFR) signaling have been reported across low-grade and high-grade glial/glioneuronal tumors. These events include structural alterations, such as gene fusions and duplications, as well as recurrent mutations in . Several FGFR-selective tyrosine kinase inhibitors (TKIs) have received regulatory approval for clinical use, and newer isoform-specific FGFR inhibitors are under investigation. Among pediatric patients with -altered low-grade gliomas (LGGs) enrolled in clinical trials with FGFR inhibitors, promising clinical efficacy regardless of alteration type (fusion or mutation) has been observed in a subset. In contrast, limited responses have been reported in adults with fused IDH-wild-type glioblastoma. FGFR inhibitor toxicities include hyperphosphatemia, diarrhea, skin, nail, and ocular toxicity. Importantly, in skeletally immature patients, bone toxicities, such as accelerated growth spurts, limb fractures, and scoliosis, have been reported and require close monitoring. Co-occurring genomic alterations in MAPK pathway signaling components downstream of FGFR may drive intrinsic and acquired resistance to FGFR inhibitors. Further preclinical studies in relevant models of FGFR-altered pediatric gliomas are needed to help inform the development of novel, more effective and less toxic treatment strategies, as well as the rational design of clinical trials. - Source: PubMed
Publication date: 2025/12/02
Sait Sameer FaroukBale TejusKarajannis Matthias A - Mitotic spindle stability is enhanced through microtubule crosslinking by a complex formed when an α helix in transforming acidic coiled-coil 3 (TACC3) binds to the helical repeats of the heavy chain of clathrin (CHC). Here, we show that the phosphorylation of TACC3 at S558 modulates the interaction by overcoming the electrostatic repulsion between K507 of CHC and basic residues in TACC3. Leveraging this insight, we optimized the sequence using peptide arrays to develop a hydrocarbon-stapled peptide (SP TACC3) that binds CHC with over 400-fold higher affinity than the native sequence, disrupting the interaction. The crystal structure of the SP TACC3-CHC complex reveals the contribution of additional polar and hydrophobic contacts to the enhanced interaction. SP TACC3 penetrates cells and displaces TACC3 from the mitotic spindle, causing a delay in mitotic progression in two out of three cancer cell lines. This work showcases a strategy for targeting the TACC3-CHC interaction with hydrocarbon-stapled peptides in a cellular context for potential cancer therapies. - Source: PubMed
Publication date: 2026/04/27
Gunning VandaBatchelor MatthewAlexander Krista KWalko MartinDill Taylor CBurgess Selena GRoyle Stephen JKennedy Eileen JBayliss Richard - KRAS G12C-mutated non-small cell lung carcinoma (NSCLC), caused by a glycine-to-cysteine substitution at codon 12, is associated with poor prognosis and is now targetable with specific inhibitors. We retrospectively analyzed 279 KRAS G12C-mutated NSCLC cases (2017-2023) from our registry with available histologic, immunohistochemical, and molecular data. The cohort included 279 patients (125 females, 151 males; mean age 67 years, range 29-91). Most tumors were primary lung carcinomas (n = 229, 82%), while 45 (16%) were metastatic at presentation. Morphologic evaluation was available in 240 tumors: 37% showed solid squamous cell carcinoma (SCC)-like features, 61% rhabdoid/plasmacytoid morphology, and 17% sarcomatoid features. Adenocarcinoma-associated patterns were present in 67 cases, often mixed, and focal solid growth occurred in 77%. TTF1, Napsin A, and CK7 were positive in 86%, 87%, and 98%, respectively, whereas squamous markers were infrequent (p40/p63 7%, CK5/6 8%). PD-L1 expression was detected in 65%. Co-mutations most commonly involved TP53 (n = 27) and STK11 (n = 12); IDH1/2, PIK3CA, and CTNNB1 mutations occurred in four cases each, MET in two cases, and BRAF, FGFR2, FGFR3, and GNAS in one case each. Two gene fusions were identified (LRP12::NRG1, FGFR3::TACC3). Mean survival was 1.89 years, with one- and five-year survival rates of 54% and 25%. KRAS G12C-mutated NSCLC is clinically aggressive and frequently shows solid growth with rhabdoid, plasmacytoid, or SCC-like morphology, which may lead to misclassification and missed genetic testing. Immunohistochemistry and molecular profiling are essential for accurate classification and enabling targeted therapy. - Source: PubMed
Publication date: 2026/04/15
Bradová MartinaSlavík PetrVaněček TomášMartínek PetrGrossmann PetrKormunda StanislavBehenská KristýnaSvatoň MartinPešek MilošJirásek Tomᚊpůrková ZuzanaHroudová PetraMrázková HanaHořavová BarboraRoubec JaromírBaník MartinMukenšnábl PetrMichal MichalŠvajdler Marián - Centrosomes organize microtubules (MT) in animal cells by recruiting a group of MT polymerization factors to the pericentriolar matrix (PCM). Tubulin enrichment within the PCM contributes to microtubule-organizing activity. However, the molecular determinants underlying this tubulin concentration remain elusive. Here, we describe a mechanism of tubulin concentration by polyKR motifs encoded in the centrosomal coiled-coil proteins. We show that polyKR sequences promote tubulin enrichment within engineered protein condensates that mimic the protein-dense environment of the centrosome. Bioinformatic analysis reveals that polyKR motif-containing coiled-coil proteins are highly enriched in centrosomes across species, from worms and flies to mice and humans. The tubulin binding affinity of polyKR motifs with six to 10 basic residues is approximately in the micromolar to submicromolar range. Cytoplasmic puncta containing the predicted centrosomal polyKR motifs concentrate microtubules. In purified systems, we show that TACC3 and Cep63 condensates containing polyKR motifs concentrate tubulin dimers over 10-fold. Moreover, the spatial density of polyKR motifs correlates with MT concentration, suggesting that cells can modulate tubulin concentration at the PCM by tuning the centrosomal composition. Our findings highlight a general function encoded in centrosomal scaffolding proteins for tubulin concentration, and this mechanism is functionally redundant to ensure robust tubulin enrichment in the PCM. - Source: PubMed
Publication date: 2026/04/03
Lin Shiou-LanChen Yu-HsunLoi Ren JunChen Yueh-TingChen TingLapouge KarineGreenan GarrettKräusslich Hans-GeorgCheng Hui-Chun