Trypanosoma cruzi is a unicellular parasite and the etiologic agent of Chagas disease. The parasite has a digenetic life cycle alternating between mammalian and insect hosts, where it faces a variety of environmental conditions to which it must adapt in order to survive. The adaptation to these changes is mediated by signaling pathways that coordinate the cellular responses to the new environmental settings. Major environmental changes include temperature, nutrient availability, ionic composition, pH, osmolarity, oxidative stress, contact with host cells and tissues, host immune response, and intracellular life. Some of the signaling pathways and second messengers potentially involved in the response to these changes have been elucidated in recent years and will be the subject of this review.
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http://dx.doi.org/10.1111/mmi.14621 | DOI Listing |
Plant Physiol Biochem
January 2025
Laboratory of Microbial Genetics, Department of Botany, Institute of Science, Banaras Hindu University, Varanasi, 221005, India. Electronic address:
Nitric oxide synthases (NOSs) are heme-based monooxygenases that catalyze the NADPH-dependent oxidation of L-arginine to produce NO and L-citrulline. Over the past five years, the identification and characterization of NOS homologs in cyanobacteria have significantly advanced our understanding of these enzymes. However, the precise mechanisms through which NOS-derived NO influences nitrogen metabolism remain incompletely elucidated.
View Article and Find Full Text PDFMedicine (Baltimore)
January 2025
Urology and Metabolic Rehabilitation Center, Beijing Rehabilitation Hospital, Capital Medical University, Xixia Zhuang, Badachu, Shijingshan District, Beijing, China.
Prostate cancer is epithelial malignant prostate hyperplasia caused by a tumor. We found prostate cancer GSE141551 and GSE200879 profiles from gene expression omnibus database, followed by differentially expressed genes (DEGs) analysis, weighted gene co-expression network analysis, protein-protein interaction analysis, gene function enrichment analysis, and comparative toxicology database analysis. Finally, the gene expression heat map was drawn, and miRNA information regulating core DEGs was retrieved.
View Article and Find Full Text PDFMedicine (Baltimore)
January 2025
Nerve Rehabilitation Center, Beijing Rehabilitation Hospital Affiliated to Capital Medical University, Xixia Zhuang, Badachu, Shijingshan District, Beijing, China.
Ischemic stroke is caused by blockage of blood vessels in brain, affecting normal function. The roles of Signal Transformer and Activator of Transcription 1 (STAT1), CASP8, and MYD88 in ischemic stroke and its care are unclear. The ischemic stroke datasets GSE16561 and GSE180470 were found from the Gene Expression Omnibus database.
View Article and Find Full Text PDFPlant Physiol
January 2025
State Key Laboratory of Medicinal Chemical Biology, Tianjin Key Laboratory of Protein Science, Frontiers Science Center for Cell Responses, College of Life Sciences, Nankai University, Tianjin, 300071, China.
The endocytic and autophagic pathways play important roles in abiotic stress responses and maintaining cellular homeostasis in plants. Asparagine Rich Proteins (NRPs) are plant-specific stress-responsive proteins that are involved in many abiotic stress-related signaling pathways. We previously demonstrated that NRP promotes PIN FORMED 2 (PIN2) vacuolar degradation to maintain PIN2 homeostasis under abscisic acid (ABA) treatment in Arabidopsis (Arabidopsis thaliana).
View Article and Find Full Text PDFPLoS Pathog
January 2025
Institute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Function-to-find domain (FIIND)-containing proteins, including NLRP1 and CARD8, are vital components of the inflammasome signaling pathway, critical for the innate immune response. These proteins exist in various forms due to autoproteolysis within the FIIND domain, resulting in full-length (FL), cleaved N-terminal (NT), and cleaved C-terminal (CT) peptides, which form autoinhibitory complexes in the steady state. However, the detailed mechanism remains elusive.
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