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The 5' N-methylguanosine cap is a critical modification for mRNAs and many other RNAs in eukaryotic cells. Recent studies have uncovered an RNA 5' capping quality surveillance mechanism, with DXO/Rai1 decapping enzymes removing incomplete caps and enabling the degradation of the RNAs, in a process we also refer to as "no-cap decay." It has also been discovered recently that RNAs in eukaryotes, bacteria, and archaea can have noncanonical caps (NCCs), which are mostly derived from metabolites and cofactors such as NAD, FAD, dephospho-CoA, UDP-glucose, UDP-N-acetylglucosamine, and dinucleotide polyphosphates. These NCCs can affect RNA stability, mitochondrial functions, and possibly mRNA translation. The DXO/Rai1 enzymes and selected Nudix (nucleotide diphosphate linked to X) hydrolases have been shown to remove NCCs from RNAs through their deNADding, deFADding, deCoAping, and related activities, permitting the degradation of the RNAs. In this review, we summarize the recent discoveries made in this exciting new area of RNA biology.
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http://dx.doi.org/10.1016/j.jbc.2022.102171 | DOI Listing |
Braz Oral Res
September 2025
Universidade de São Paulo - USP, Bauru School of Dentistry, Department of Biological Sciences, Bauru, SP, Brazil.
Angiotensin II (Ang II) releases inflammatory mediators from several cell types. The objective of this study was to investigate the potential of Ang II to induce mRNA expression of inflammatory mediators in primary cultured fibroblast-like cells isolated from gingival and periodontal ligament tissues. A synergistic effect of co-treatment with Ang II and Interleukin-1β (IL1β) on the mRNA expression of inflammatory mediators was explored.
View Article and Find Full Text PDFPLoS One
September 2025
Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Crosstalk between leukemic cells and their surrounding mesenchymal stromal cells (MSCs) in the bone marrow microenvironment is crucial for the pathogenesis of myelodysplastic syndromes (MDS) and is mediated by extracellular vesicles (EVs). The EV-specific miRNAs derived from MDS-MSCs remain poorly explored. EVs isolated from HS-5, an immortalized stromal cell line, promoted the proliferation and 5-azacytidine (AZA) resistance of SKM-1 cells.
View Article and Find Full Text PDFSci Adv
September 2025
Department of Bioengineering and Therapeutic Sciences, University of California, San Francisco, San Francisco, CA, USA.
Breastfeeding is essential for reducing infant morbidity and mortality, yet exclusive breastfeeding rates remain low, often because of insufficient milk production. The molecular causes of low milk production are not well understood. Fresh milk samples from 30 lactating individuals, classified by milk production levels across postpartum stages, were analyzed using genomic and microbiome techniques.
View Article and Find Full Text PDFSci Transl Med
September 2025
Key Laboratory of Breast Cancer in Shanghai, Department of Breast Surgery, Precision Cancer Medicine Center, Fudan University Shanghai Cancer Center, Shanghai 200032, P. R. China.
Triple-negative breast cancers (TNBCs) lack predictive biomarkers to guide immunotherapy, especially during early-stage disease. To address this issue, we used single-cell RNA sequencing, bulk transcriptomics, and pathology assays on samples from 171 patients with early-stage TNBC receiving chemotherapy with or without immunotherapy. Our investigation identified an enriched subset of interferon (IFN)-induced CD8 T cells in early TNBC samples, which predict immunotherapy nonresponsiveness.
View Article and Find Full Text PDFSci Transl Med
September 2025
Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
IFN-β, a type I interferon, has been used as a first-line therapy for patients with multiple sclerosis (MS) for more than 30 years; however, the cellular and molecular basis of its therapeutic efficacy remains unclear. Here, we first used experimental autoimmune encephalomyelitis (EAE), a mouse model for MS, to show that the therapeutic effects of IFN-β were associated with a down-regulation of microRNA-21 (miR-21) and pathogenic T17 (pT17) cells. In vitro experiments demonstrated that genetic knockout of miR-21 directly inhibited pathogenic T17 cell differentiation.
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