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Adenosine deaminase acting on RNA 1 (ADAR1) plays an essential role in the development of malignancies by modifying the expression of different oncogenes. ADAR1 presents three distinct activities: adenosine-to-inosine RNA editing, modulating IFN pathways, and response to cellular stress factors. Following stressors such as heat shock, ADAR1p110 isoform relocates from the nucleus to the cytoplasm, where it suppresses RNA degradation which leads to the arrest of apoptosis and cell survival. In this study, we assessed the expression of ADAR1 across different cancer cell lines. We revealed that the presence of ADAR1 varies between cells of different origins and that a high transcript level does not reflect protein abundance. Additionally, we subjected cells to a heat shock in order to evaluate how cellular stress factors affect the expression of ADAR1. Our results indicate that ADAR1 transcript and protein levels are relatively stable and do not change under heat shock in examined cell lines. This research lays a groundwork for future directions on ADAR1-related studies suggesting in which types of cancer ADAR1 may be a promising target for novel therapeutic approaches.
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http://dx.doi.org/10.1007/s13353-024-00926-4 | DOI Listing |
Biomed Pharmacother
September 2025
Department of Biomedical Sciences, Institute of Health, Jimma University, Jimma 378, Ethiopia; Division of Research & Development, Lovely Professional University, Phagwara 144411, India. Electronic address:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterised by cognitive decline and the accumulation of misfolded proteins, including amyloid-beta and hyperphosphorylated tau, which impair neuronal function and promote cell death. These misfolded proteins disrupt proteostasis by forming toxic aggregates that exacerbate disease progression. Molecular chaperones, such as heat shock proteins, actively maintain protein homeostasis by assisting in proper folding, preventing aggregation, and promoting the clearance of misfolded proteins.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba 305-8577, Japan.
All organisms are exposed to various stressors, which can sometimes lead to organismal death, depending on their intensity. While stress-induced organismal death has been observed in many species, the underlying mechanisms remain unclear. In this study, we investigated the molecular mechanisms of stress-induced organismal death in the fruit fly .
View Article and Find Full Text PDFJCI Insight
September 2025
Division of Metabolism, Endocrinology & Diabetes, and.
Intracellular trafficking of secretory and membrane proteins from the endoplasmic reticulum (ER) to the cell surface, via the secretory pathway, is crucial to the differentiated function of epithelial tissues. In the thyroid gland, a prerequisite for such trafficking is proper protein folding in the ER, assisted by an array of ER molecular chaperones. One of the most abundant of these chaperones, Glucose-Regulated-Protein-170 (GRP170, encoded by Hyou1), is a noncanonical hsp70-like family member.
View Article and Find Full Text PDFZool Res
September 2025
Department of Urology & Andrology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310016, China. E-mail:
Chromatin remodeling and transcriptional reprogramming play critical roles during mammalian meiotic prophase I; however, the precise mechanisms regulating these processes remain poorly understood. Our previous work demonstrated that deletion of heat shock factor 5 (HSF5), a member of the heat shock factor family, induces meiotic arrest and male infertility. However, the molecular pathways through which HSF5 governs meiotic progression have not yet been fully elucidated.
View Article and Find Full Text PDFDevelopment
September 2025
Department of Molecular & Cell Biology, University of California, Berkeley, CA 94720, USA.
Organ initiation is often driven by extracellular signaling molecules that activate precursor cells competent to receive and respond to a given signal, yet little is known about the dynamics of competency in space and time during development. Teeth are excellent organs to study cellular competency because they can be activated with the addition of a single signaling ligand, Ectodysplasin (Eda). To investigate the role of Eda in tooth specification, we generated transgenic sticklebacks and zebrafish with heat shock-inducible Eda overexpression.
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