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RNA helicases, the largest family of proteins that participate in RNA metabolism, stabilize the intracellular environment through various processes, such as translation and pre-RNA splicing. These proteins are also involved in some diseases, such as cancers and viral diseases. Autophagy, a self-digestive and cytoprotective trafficking process in which superfluous organelles and cellular garbage are degraded to stabilize the internal environment or maintain basic cellular survival, is associated with human diseases. Interestingly, similar to autophagy, RNA helicases play important roles in maintaining cellular homeostasis and are related to many types of diseases. According to recent studies, RNA helicases are closely related to autophagy, participate in regulating autophagy, or serve as a bridge between autophagy and other cellular activities that widely regulate some pathophysiological processes or the development and progression of diseases. Here, we summarize the most recent studies to understand how RNA helicases function as regulatory proteins and determine their association with autophagy in various diseases.
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http://dx.doi.org/10.1631/jzus.B2000245 | DOI Listing |
Alzheimers Res Ther
September 2025
Department of Neurology, Saarland University, Kirrberger Straße, 66421, Homburg/Saar, Germany.
Background: Alzheimer's disease (AD) patients and animal models exhibit an altered gut microbiome that is associated with pathological changes in the brain. Intestinal miRNA enters bacteria and regulates bacterial metabolism and proliferation. This study aimed to investigate whether the manipulation of miRNA could alter the gut microbiome and AD pathologies.
View Article and Find Full Text PDFNucleic Acids Res
September 2025
Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208, United States.
DDX6 is known to repress messenger RNA (mRNA) translation and promote mRNA decay in microRNA-mediated silencing. In embryonic stem cells (ESCs), DDX6 primarily functions at the translation level, independent of mRNA destabilization; however, the precise molecular mechanism of how DDX6 represses translation remains unclear. Here, we identify DDX3X as a key downstream target of DDX6-mediated translational repression in ESCs.
View Article and Find Full Text PDFGen Physiol Biophys
September 2025
The Second Department of Nephrology, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Diabetic nephropathy (DN) is a major complication of diabetes, imposing substantial socioeconomic and public health challenges. N6-methyladenosine (m6A) modification, a prevalent epigenetic mechanism, influences cellular processes and disease progression. Wilms' tumor 1-associating protein (WTAP), an m6A methyltransferase subunit, was investigated for its role in DN.
View Article and Find Full Text PDFBlood Adv
September 2025
Institut de Recherches Cliniques de Montreal - IRCM, Montreal, Quebec, Canada.
Acute myeloid leukemia (AML) with rearrangement of the mixed lineage leukemia gene express MLL-AF9 fusion protein, a transcription factor that impairs differentiation and drives expansion of leukemic cells. We report here that the zinc finger protein GFI1 together with the histone methyltransferase LSD1 occupies the promoter and regulates expression of the lncRNA ELDR in the MLL-r AML cell line THP-1. Forced ELDR overexpression enhanced the growth inhibition of an LSD1i/ATRA combination treatment and reduced the capacity of these cells to generate leukemia in xenografts, leading to a longer leukemia-free survival.
View Article and Find Full Text PDFMol Cell
September 2025
Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Dr. Bohr-Gasse 3, 1030 Vienna, Austria. Electronic address:
PIWI-clade Argonaute proteins and their associated PIWI-interacting RNAs (piRNAs) are essential guardians of genome integrity, silencing transposable elements through distinct nuclear and cytoplasmic pathways. Nuclear PIWI proteins direct heterochromatin formation at transposon loci, while cytoplasmic PIWIs cleave transposon transcripts to initiate piRNA amplification. Both processes rely on target RNA recognition by PIWI-piRNA complexes, yet how this leads to effector recruitment is unclear.
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