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In this study, we further investigated a previously developed aptamer targeting ROS 17/2.8 (rat osteosarcoma) cells. We found that this C6-8 aptamer specifically binds to heterogeneous nuclear ribonucleoprotein (hnRNP) A2/B1 and that it specifically labeled multiple tumor-cell lines as effectively as hnRNP A2/B1 monoclonal antibodies. When conjugated with fluorescent carbon nanodots (CDots) it could freely enter multiple living tumor cell lines (HepG2, MCF-7, H1299, and HeLa), whose growth it inhibited by targeting hnRNP A2/B1. Similar inhibitory effects were observed when the GFP-HepG2 hepatocarcinoma cells treated with C6-8-conjugated CDots were implanted in nude mice. Our work provides a new aptamer for targeting/labeling multiple tumor cell types, and its nanoparticle conjugates bring further advantages that increase its potential for use in cancer diagnosis and therapy.
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http://dx.doi.org/10.1016/j.biomaterials.2015.06.013 | DOI Listing |
Sci Adv
August 2025
Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
The pseudouridine synthase DKC1 regulates internal ribosome entry site (IRES)-dependent translation and is up-regulated in cancers by the MYC family of oncogenes. The functional significance of DKC1 up-regulation and the mechanistic connection between pseudouridylation and IRES-mediated translation remain poorly understood. Here, we report that DKC1 drives an ATF4-mediated transcriptional program that supports amino acid metabolism and stress adaptation.
View Article and Find Full Text PDFJ Cell Biol
October 2025
Division of Regenerative Medicine, Research Center for Medical Sciences, The Jikei University School of Medicine, Tokyo, Japan.
TDP-43, an RNA-binding protein (RBP) encoded by the TARDBP gene, is crucial for understanding the pathogenesis of neurodegenerative diseases like amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration. Dysregulated TDP-43 causes motor neuron loss, highlighting the need for proper expression levels. Here, we identify a dominant-negative isoform among the multiple TARDBP splicing variants and validate its endogenous expression using a developed antibody against its translated product.
View Article and Find Full Text PDFCNS Neurosci Ther
August 2025
The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Aims: Sevoflurane can aggravate the progression of neurodegeneration, although the underlying mechanisms remain incompletely understood. Our previous study identified a link between heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) and sevoflurane-induced neurocognitive impairments. The abnormal hydrogel phase transition of stress granules (SGs) assembled via liquid-liquid phase separation (LLPS) by hnRNPA2/B1 is a crucial element in neurodegeneration.
View Article and Find Full Text PDFAlzheimers Dement
August 2025
Department of Translational Neuroscience, Barrow Neurological Institute, Phoenix, Arizona, USA.
Introduction: Splicing protein mislocalization is associated with tau pathogenesis, but its role in Down syndrome (DS) is under-investigated.
Methods: Spliceosome associations with tau and plaque pathology were examined in frontal cortex from DS with dementia (DSD+) and without dementia (DSD-) using quantitative immunoblotting and immunohistochemistry.
Results: U1-70K and U1A levels were downregulated, and hnRNPA2B1, 3Rtau, and 4Rtau were upregulated, whereas SRSF2 and CLK1 were unchanged in DSD+.
Cell Mol Life Sci
August 2025
Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, 48940, Spain.
Oligodendrocyte dysfunction, myelin degeneration, and white matter changes are critical events in the cognitive decline of Alzheimer's disease (AD). Amyloid-β peptide (Aβ), a hallmark of AD, disrupts oligodendrocyte and myelin homeostasis, through mechanisms that remain poorly understood. Here, transcriptomic profiling of Aβ-exposed oligodendrocytes revealed widespread gene expression changes, particularly in RNA-related processes.
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