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| http://dx.doi.org/10.1093/rap/rkae122 | DOI Listing |
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MicroRNA-155 Inhibition Activates Wnt/β-catenin Signaling to Restore Th17/Treg Balance and Protect against Acute Ischemic Stroke.
eNeuro
January 2025
Department of Neurology, Quanzhou First Hospital Affiliated to Fujian Medical University, Quanzhou 362002, China.
Acute ischemic stroke (AIS) is a dangerous neurological disease associated with an imbalance in Th17/Treg cells and abnormal activation of the Wnt/β-catenin signaling pathway. This study aims to investigate whether inhibition of miR-155 can activate the Wnt/β-catenin signaling pathway to improve Th17/Treg imbalance and provide neuroprotective effects against stroke. We employed a multi-level experimental design.
View Article and Find Full Text PDFHuman TRMT1 and TRMT1L paralogs ensure the proper modification state, stability, and function of tRNAs.
Cell Rep
January 2025
Department of Biology, Center for RNA Biology, University of Rochester, Rochester, NY, USA. Electronic address:
The tRNA methyltransferase 1 (TRMT1) enzyme catalyzes the N2,N2-dimethylguanosine (m2,2G) modification in tRNAs. Intriguingly, vertebrates encode an additional tRNA methyltransferase 1-like (TRMT1L) paralog. Here, we use a comprehensive tRNA sequencing approach to decipher targets of human TRMT1 and TRMT1L.
View Article and Find Full Text PDFNtLPA1 overexpression regulates the growth of tobacco and enhances resistance to blight.
Transgenic Res
January 2025
Shaanxi Tobacco Company Baoji City Company, Baoji, 721000, Shaanxi, China.
The involvement of Loose Plant Architecture 1 (LPA1) in regulating plant growth and leaf angle has been previously demonstrated. However, the fundamental genetic background remains unidentified. To further understand the tissue expression profile of the NtLPA1 gene, an overexpression vector (pBI121-NtLPA1) was developed and employed to modify tobacco using the leaf disc method genetically.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
Janssen Research & Development, A Division of Janssen Pharmaceutica, Neuroscience Therapeutic Area, Beerse, Belgium.
Background: Neurodegenerative diseases are a heterogeneous group of illnesses. Differences across patients exist in the underlying biological drivers of disease. Furthermore, cross-diagnostic disease mechanisms exist, and different pathologies often co-occur in the brain.
View Article and Find Full Text PDFBackground: The earliest recognized biomarker of AD is deposition of Aβ amyloid that leads to formation of plaques and may, over time, trigger or at least be followed by gliosis/neuroinflammation and neurofibrillary tangles, accompanied by neurodegenerative changes including neuronal and synaptic loss. We have previously reported that semaphorin 4D (SEMA4D), the major ligand of plexin B receptors expressed on astrocytes, is upregulated in diseased neurons during progression of AD and Huntington's disease (HD). Binding of SEMA4D to PLXNB receptors triggers astrocyte reactivity, leading to loss of neuroprotective homeostatic functions, including downregulation of glutamate and glucose transporters (doi:10.
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