Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1200/PO-24-00694 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Targeted hotspot profiling reveals a functionally relevant mutation in bladder cancer.
Urol Oncol
September 2025
Nutritional, Genes and Human Disease Laboratory, Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, Bangladesh. Electronic address:
Background: Understanding the mutational landscape is critical for elucidating the molecular mechanisms driving cancer progression. This study aimed to profile somatic mutations in bladder cancer patients (N=7) from Bangladesh to provide insights into the genetic alterations underlying this malignancy.
Methods: We performed targeted sequencing of 50 oncogenes and tumor suppressor genes using the Ion AmpliSeq Cancer Hotspot Panel v2 on tumor and matched blood samples from seven bladder cancer patients.
Autophosphorylation of conserved yeast and human casein kinase 1 isozymes regulates Elongator-dependent tRNA modifications.
Nucleic Acids Res
September 2025
Department of Microbiology, Institute of Biology, University of Kassel, 34132 Kassel, Germany.
Casein kinase 1 (CK1) family members are crucial for ER-Golgi trafficking, calcium signalling, DNA repair, transfer RNA (tRNA) modifications, and circadian rhythmicity. Whether and how substrate interactions and kinase autophosphorylation contribute to CK1 plasticity remains largely unknown. Here, we undertake a comprehensive phylogenetic, cellular, and molecular characterization of budding yeast CK1 Hrr25 and identify human CK1 epsilon (CK1ϵ) as its ortholog.
View Article and Find Full Text PDFA pathological role of O-GlcNAcylation-driven TR11B production and function in lung adenocarcinoma.
Dev Cell
September 2025
Department of Clinical Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Faculty of Medical Laborat
Cytokines link inflammation to tumorigenesis, but the role of post-translational modifications in regulating their function within the extra-tumoral environment remains poorly defined. Here, we identify tumor-derived tumor necrosis factor (TNF) receptor superfamily member 11B (TR11B) as a key driver of lung adenocarcinoma (LUAD) progression and therapeutic resistance. Mechanistically, O-GlcNAc transferase (OGT)-mediated O-GlcNAcylation at serine 151 stabilizes TR11B and facilitates its interaction with the membrane protein EPS15 homology domain-containing protein 1 (EHD1), promoting cyclin dependent kinase 2 (CDK2) phosphorylation and cell cycle progression.
View Article and Find Full Text PDFMetformin attenuates coal dust nanoparticle-induced pulmonary fibrosis by modulating inflammation and epithelial-mesenchymal transition.
Int Immunopharmacol
September 2025
The First Hospital of Anhui University of Science and Technology, Huainan 232000, China; Bengbu Medical University, Bengbu 233030, China. Electronic address:
Coal worker pneumoconiosis is an occupational pulmonary fibrosis (PF) caused by prolonged exposure to respirable coal dust (CD), with limited therapeutic options. Here, we explored the antifibrotic effects of metformin (Met) in CD-nanoparticle (CD-NP)-induced PF, focusing on its preventive and therapeutic potential. In vivo, Met was administered at different doses (low: 31.
View Article and Find Full Text PDFRas/Raf dimerization model for activation of Raf kinase.
Curr Opin Struct Biol
September 2025
Department of Chemistry and Chemical Biology, Northeastern University, 360 Huntington Ave, Boston, MA 02115, USA. Electronic address:
Our previously proposed Ras dimerization model is consistent with recent details observed by NMR in that Raf activation is centered on the Ras/Raf dimer, distinct from one in which Ras activates Raf as a monomer with the Raf cysteine rich domain inserted in the membrane. We review mechanistic understanding of Raf activation within nanoclusters of Ras on the membrane, with a shift to dimers upon binding Raf. This sets the stage for a signaling platform composed of Ras/Raf and Galectin dimers that facilitates the release of Raf autoinhibition and folding of the Raf intrinsically disordered region between the Ras-binding domains and the kinase bound to 14-3-3 and MEK.
View Article and Find Full Text PDF