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A stress paradox: the dual role of the unfolded protein response in the placenta.
Front Endocrinol (Lausanne)
December 2024
Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada.
The placenta is a temporary organ that forms during pregnancy and is essential for fetal development and maternal health. As an endocrine organ, proper placental function requires continual production, folding, and transport of proteins and lipids. Central to these processes is the endoplasmic reticulum (ER), a dynamic organelle responsible for maintaining cellular protein and lipid synthesis and processing.
View Article and Find Full Text PDFLight-Controlled Intracellular Synthesis of Poly(luciferin) Polymers Induces Cell Paraptosis.
J Am Chem Soc
January 2025
Department of Radiology, Molecular Imaging Program at Stanford, Stanford University School of Medicine, Stanford, California 94305, United States.
Accumulation of misfolded proteins challenges cellular proteostasis and is implicated in aging and chronic disorders. Cancer cells, moreover, face an elevated level of basal proteotoxic stress; hence, exacerbating endoplasmic reticulum (ER) stress has been shown to induce programmed cell death while enhancing anticancer immunogenicity. We hypothesize that hydrophobic abiotic macromolecules can trigger a similar stress response.
View Article and Find Full Text PDFeIF2α Phosphorylation-ATF4 Axis-Mediated Transcriptional Reprogramming Mitigates Mitochondrial Impairment During ER Stress.
Mol Cells
January 2025
Basic-Clinical Convergence Research Center, School of Biological Sciences, University of Ulsan, Ulsan 44610, Korea. Electronic address:
Eukaryotic translation initiation factor 2α (eIF2α) phosphorylation, which regulates all three unfolded protein response pathways, helps maintain cellular homeostasis and overcome endoplasmic reticulum (ER) stress through transcriptional and translational reprogramming. However, transcriptional regulation of mitochondrial homeostasis by eIF2α phosphorylation during ER stress is not fully understood. Here, we report that the eIF2α phosphorylation-activating transcription factor 4 (ATF4) axis is required for expression of multiple transcription factors (TFs) including nuclear factor erythroid 2-related factor 2 (Nrf2) and their target genes responsible for mitochondrial homeostasis during ER stress.
View Article and Find Full Text PDFPseudorabies virus inhibits the unfolded protein response for viral replication during the late stages of infection.
Vet Microbiol
December 2024
National Key Laboratory of Veterinary Public Health and Safety, Key Laboratory of Animal Epidemiology of the Ministry of Agriculture and Rural Affairs, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
Pseudorabies virus (PRV) poses a significant threat to the global swine breeding industry and public health, but how the virus transverses the host defense systems for efficient viral replication and pathogenesis remains unclear. Here, we report that PRV could inhibit the unfolded protein response (UPR), a critical component of host innate immunity against viral infection, to promote virus replication during the late infection stages. PERK was shown phosphorylated and active in PRV-infected cells, but the subsequent events were suppressed post virus infection, such as eIF2α phosphorylation, ATF4 expression, and the formation of stress granules (SGs).
View Article and Find Full Text PDFHypoxia promotes tumor immune evasion by suppressing MHC-I expression and antigen presentation.
EMBO J
January 2025
Department of Oncology, The University of Oxford, Oxford, OX3 7DQ, UK.
Hypoxia is a common feature of solid tumors that has previously been linked to resistance to radiotherapy and chemotherapy, and more recently to immunotherapy. In particular, hypoxic tumors exclude T cells and inhibit their activity, suggesting that tumor cells acquire a mechanism to evade T-cell recognition and killing. Our analysis of hypoxic tumors indicates that hypoxia downregulates the expression of MHC class I and its bound peptides (i.
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