Ask about this productRelated genes to: RBM10 antibody
- Gene:
- RBM10 NIH gene
- Name:
- RNA binding motif protein 10
- Previous symbol:
- -
- Synonyms:
- DXS8237E, KIAA0122, GPATC9, ZRANB5, GPATCH9, S1-1
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-21
- Date modifiied:
- 2018-10-16
Related products to: RBM10 antibody
Related articles to: RBM10 antibody
- RNA-binding motif 10 (RBM10) mutation in non-small-cell lung cancer (NSCLC) is associated with decreased sensitivity to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors in vitro and in patients who received osimertinib as neoadjuvant treatment or palliative systemic therapy. The incidence of this mutation in early-stage NSCLC and the relationship with other mutations are unknown. - Source: PubMed
Publication date: 2026/03/10
Suda KenichiSakai KazukoIto MasaokiOiki HanaFukuda ShotaOhara ShutaHamada AkiraChiba MasatoShimoji MasakiNishio KazutoTsutani Yasuhiro - ERBB2 mutations occur in 1-4% of all non-small cell lung cancers (NSCLCs). Trastuzumab-deruxtecan and the novel ERBB2 tyrosine kinase inhibitors zongertinib and sevabertinib are FDA-approved for the treatment of metastatic ERBB2-mutant NSCLC based on data from tumors harboring tyrosine kinase domain (TKD) mutations. The clinico-genomic characteristics of NSCLC tumors with ERBB2 mutations beyond the TKD remain largely unexplored. - Source: PubMed
Publication date: 2026/04/01
Stockhammer PaulEl Zarif TalalSchillo Jacob LLi FangyongGoldberg Sarah BPoliti KaterinaGrant Michael J - Pair correlation function (pCF) is a powerful approach that has gained increasing popularity in recent years for studying protein dynamics in living cells; however, its application remains limited by methodological constraints and the absence of standardized protocols. In this work, we optimize key aspects of pCF and dual color-pCF analysis, showing that reliable results can be achieved with shorter acquisition times, reducing motion artifacts. We demonstrate that spectral bleed-through as low as 1% produces spurious cross-correlations, underscoring the need for rigorous correction. To address this, we introduce a robust signal demixing strategy that removes false-positive correlations while preserving genuine molecular interactions. This advance expands the reliability of correlation analyses in complex live-cell environments. Applying this approach, we investigate the nucleo-cytoplasmic shuttling of the splicing factor RBM10 in living cells expressing dengue virus (DENV) NS5 polymerase under poly(I:C)-triggered innate immune response. Our findings reveal that RBM10 and NS5 not only interact but also co-shuttle between the nuclear and cytoplasmic compartments. Furthermore, RBM10 transport is differentially modulated by both NS5 and innate immune induction, reinforcing the role of DENV in altering host nuclear transport. Overall, this work establishes signal demixing as a key advance for live-cell correlation techniques and demonstrates its potential for uncovering complex host-virus interactions. - Source: PubMed
Publication date: 2026/04/02
Philipp NataliaMagalnik MelinaPozzi BertaSrebrow AnabellaEstrada Laura C - Although mesenchymal-epithelial transition proto-oncogene ( amplification is a common resistance mechanism in targeted therapy for lung cancer, rapid disease progression associated with this resistance mechanism in patients with epidermal growth factor receptor () mutation has scarcely been reported. Herein, we report a fatal case of lung adenocarcinoma that rapidly progressed after failure of EGFR-tyrosine kinase inhibitor treatment following the emergence of amplification. A 62-year-old man was diagnosed with metastatic lung adenocarcinoma containing mutations in exon L858R and RNA-binding motif 10. He received afatinib as frontline treatment and showed a partial response; however, the right lung lesion progressed after 14 months of treatment. Although the drug was maintained after salvage segmentectomy of the lesion, lung nodules and pleural effusion developed shortly thereafter. Because testing using resected tissue showed only the original mutation, we switched his regimen to pemetrexed and carboplatin. However, the disease rapidly progressed with a very large mass in the right lung and massive pleural effusion, which led to death within 7 weeks of treatment. Next-generation sequencing was performed at the time of first progression and second progression revealed acquired amplification (copy number gain 15.5 and 9.1, respectively) in addition to baseline mutations. Although an association between amplification and rapidly progressive lung cancer has been predicted previously, to the best of our knowledge, this is the first report on the potential contribution of other mutations, such as those in RNA-binding motif 10, during -driven rapid progression. Our report highlights the importance of more active utilization of molecular profiling for the emergence of resistance during tyrosine kinase inhibitor use and the early identification of MET amplification and timely initiation of MET-targeted therapy, such as MET inhibitors in combination with EGFR-TKIs, to potentially mitigate rapid disease progression and clinical deterioration. - Source: PubMed
Publication date: 2026/01/29
Kim JiwonNa KiyongLee Seung Hyeun - - Source: PubMed
Publication date: 2026/03/23
Zhang Xiang-YuChen Huan-HuanZhu Yue-FengHu Si-YuanZhang HuanCui Ya-XinYang JinShen Chen-Yang