Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Non-coding small RNAs and Argonaute proteins mediate conserved defenses against foreign genetic elements. mutants in the insulin/IGF-1 signaling (IIS) have previously been shown to exhibit an enhanced response to exogenous RNAi. Here, we found that the loss of IIS via enhances transgene silencing, which is reversed by knocking out . Similarly, mutants show enhanced RNAi and upregulation of antiviral RNAi pathway. and mutations exhibit additive effects, and loss of restores transgene expression in mutants but not in mutants, suggesting that these genes act in parallel. RNAi gene expression in mutants lacked a consistent pattern, suggesting IIS may regulate RNAi components via post-translational mechanisms.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12368607 | PMC |
| http://dx.doi.org/10.17912/micropub.biology.001747 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Reduced insulin/IGF-1 signaling and loss of promote repetitive DNA silencing in .
MicroPubl Biol
August 2025
School of Neurobiology, Biochemistry and Biophysics, Wise Faculty of Life Sciences & Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Tel Aviv, Israel.
Non-coding small RNAs and Argonaute proteins mediate conserved defenses against foreign genetic elements. mutants in the insulin/IGF-1 signaling (IIS) have previously been shown to exhibit an enhanced response to exogenous RNAi. Here, we found that the loss of IIS via enhances transgene silencing, which is reversed by knocking out .
View Article and Find Full Text PDFMicrobial Lipopolysaccharide Regulates Host Development Through Insulin/IGF-1 Signaling.
Int J Mol Sci
July 2025
Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai 200438, China.
Lipopolysaccharide (LPS), the defining outer membrane component of Gram-negative bacteria, is a potent immunostimulant recognized by Toll-like receptor 4 (TLR4). While extensively studied for its roles in immune activation and barrier disruption, the potential function of LPS as a developmental cue remains largely unexplored. By leveraging and its genetic and gnotobiotic advantages, we screened a panel of LPS biosynthesis mutants.
View Article and Find Full Text PDFGene Monitoring in Obesity-Induced Metabolic Dysfunction in Rats: Preclinical Data on Breast Neoplasia Initiation.
Int J Mol Sci
July 2025
Department of Gynecology and Obstetrics, School of Medical Sciences, State University of Campinas (UNICAMP), Campinas 13083-887, Brazil.
Obesity and metabolic dysfunction are established risk factors for luminal breast cancer, yet current preclinical models inadequately recapitulate the complex metabolic and immune interactions driving tumorigenesis. To develop and characterize an immunocompetent rat model of luminal breast cancer induced by chronic exposure to a cafeteria diet mimicking Western obesogenic nutrition, female rats were fed a cafeteria diet or standard chow from weaning. Metabolic parameters, plasma biomarkers (including leptin, insulin, IGF-1, adiponectin, and estrone), mammary gland histology, tumor incidence, and gene expression profiles were longitudinally evaluated.
View Article and Find Full Text PDFCondition-dependent effects of knockdown of autophagy on longevity.
bioRxiv
July 2025
Institute of Healthy Ageing, and Research Department of Genetics, Evolution and Environment, University College London, London, UK.
Autophagy is thought to clear damaged cellular constituents that contribute to aging, and several life-extending interventions in model organisms show some degree of autophagy dependence. In , inhibiting autophagy can shorten, lengthen or have no effect on lifespan. Differences between published findings likely reflect variability in experimental conditions.
View Article and Find Full Text PDFMolecular and Environmental Modulators of Aging: Interplay Between Inflammation, Epigenetics, and RNA Stability.
Genes (Basel)
July 2025
Department of Biochemistry and Biotechnology, University of Thessaly, Biopolis, 415 00 Larissa, Greece.
Aging is a complex biological process characterized by the progressive accumulation of cellular and molecular damage, leading to functional decline and increased susceptibility to age-related diseases. Central to this process is cellular senescence, a state of irreversible cell cycle arrest that acts as both a protective mechanism against tumorigenesis and a contributor to tissue degeneration. Herein, we explore the genetic and molecular mechanisms underlying aging, with a focus on telomere dynamics, the gene, angiotensin-converting enzyme (ACE), and the NF-κB pathway.
View Article and Find Full Text PDF