neuronal RNAi does not render other tissues refractory to RNAi.

Proc Natl Acad Sci U S A

Department of Biological Sciences, Indian Institute of Science Education and Research, Mohali, Punjab 140306, India.

Published: May 2024


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11145236PMC
http://dx.doi.org/10.1073/pnas.2401096121DOI Listing

Publication Analysis

Top Keywords

neuronal rnai
4
rnai render
4
render tissues
4
tissues refractory
4
refractory rnai
4
neuronal
1
render
1
tissues
1
refractory
1
rnai
1

Similar Publications

Splicing factor Nova regulates the splice variants in exons 3 and 6 of GABA receptor subunit RDL from Chilo suppressalis Walker (Lepidoptera: Crambidae).

Pestic Biochem Physiol

November 2025

State Key Laboratory of Agricultural and Forestry Biosecurity, College of Plant Protection, Nanjing Agricultural University, Nanjing 211800, PR China. Electronic address:

The insect ionotropic γ-aminobutyric acid (GABA) receptor is an important insecticide target, and alternative splicing (AS) among exons 3a, 3b, 6a, and 6b of its RDL subunit is ubiquitous in insects; however, the AS factors and mechanisms remain unclear. While the neuro-oncological ventral antigen (Nova) is known to regulate AS of the γ2 subunit of mammalian GABA receptors, its role in insects remains unexplored. Two CsNova isoforms, CsNova-X1 and CsNova-X3, were identified by BLAST in the third-generation transcriptome of Chilo suppressalis.

View Article and Find Full Text PDF

Huntington's disease (HD) is a progressive, autosomal dominant neurodegenerative disorder characterized by motor dysfunction, cognitive decline, and psychiatric disturbances. It is caused by CAG repeat expansions in the HTT gene, resulting in the formation of mutant huntingtin protein that aggregates and disrupts neuronal function. This review outlines the pathogenesis of HD, including genetic, molecular, and environmental factors.

View Article and Find Full Text PDF

Olfactory Molecular Mechanism Study on the Recognition of the Danger Signal 1-Octen-3-ol in the Parasitic Wasp .

J Agric Food Chem

September 2025

Jilin Provincial Key Laboratory of Animal Resource Conservation and Utilization, School of Life Sciences, Northeast Normal University, Changchun 130024, China.

The odor-driven behavior of parasitoids critically determines their efficacy as biological control agents. Although host-seeking mechanisms are well studied, little is known about their danger signal detection capacity. Here, we studied the synergistic action of odorant binding proteins (OBPs) and odorant receptors (ORs) while detecting the repellence of 1-octen-3-ol in .

View Article and Find Full Text PDF

This study aimed to investigate the effects of caffeoylquinic acids from Erigeron breviscapus(EBCQA) on cognitive impairment and mitochondrial dysfunction in Alzheimer's disease(AD), and to explore its underlying mechanisms. The impacts of EBCQA on paralysis, β-amyloid(Aβ) oligomerization, and mRNA expression of mitophagy-related genes [PTEN-induced putative kinase 1(PINK1) homolog-encoding gene pink-1, Parkin homolog-encoding gene pdr-1, Bcl-2 interacting coiled-coil protein 1(Beclin 1) homolog-encoding gene bec-1, microtubule-associated protein 1 light chain 3(LC3) homolog-encoding gene lgg-1, autophagic adapter protein 62(p62) homolog-encoding gene sqst-1] were examined in the AD Caenorhabditis elegans CL4176 model, along with mitochondrial functions including adenosine triphosphate(ATP) content, enzyme activities of mitochondrial respiratory chain complexes Ⅰ,Ⅲ, and Ⅳ, and mitochondrial membrane potential. Additionally, the effects of EBCQA on the green fluorescent protein(GFP)/red fluorescent protein from Discosoma sp.

View Article and Find Full Text PDF

Dihydroceramide desaturases convert dihydroceramides to ceramides, the precursors of all complex sphingolipids. Reduction of DEGS1 dihydroceramide desaturase function causes pediatric neurodegenerative disorder hypomyelinating leukodystrophy-18 (HLD-18). We discovered that (), the homolog, is expressed primarily in glial cells to promote CNS development by guarding against neurodegeneration.

View Article and Find Full Text PDF