The epidemic of pulmonary tuberculosis (TB), especially rifampin-resistant tuberculosis (RR-TB) presents a major challenge for TB control today. However, there is a lack of reliable and specific biomarkers for the early diagnosis of RR-TB. We utilized reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to profile the transcript levels of 72 tripartite motif (TRIM) genes from a discovery cohort of 10 drug-sensitive tuberculosis (DS-TB) patients, 10 RR-TB patients, and 10 healthy controls (HCs). A total of 35 differentially expressed genes (DEGs) were screened out, all of which were down-regulated. The bio functions and pathways of these DEGs were enriched in protein ubiquitination, regulation of the viral process, Interferon signaling, and innate immune response, etc. A protein-protein interaction network (PPI) was constructed and analyzed using STRING and Cytoscape. Twelve TRIM genes were identified as hub genes, and seven (TRIM1, 9, 21, 32, 33, 56, 66) of them were verified by RT-qPCR in a validation cohort of 95 subjects. Moreover, we established the RR-TB decision tree models based on the 7 biomarkers. The receiver operating characteristic (ROC) analyses showed that the models exhibited the areas under the curve (AUC) values of 0.878 and 0.868 in discriminating RR-TB from HCs and DS-TB, respectively. Our study proposes potential biomarkers for RR-TB diagnosis, and also provides a new experimental basis to understand the pathogenesis of RR-TB.
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http://dx.doi.org/10.1016/j.micpath.2021.104916 | DOI Listing |
Genetics
January 2025
Department of Molecular Genetics, University of Toronto, 661 University Avenue, Toronto, Ontario, Canada M5G 1M1.
The Drosophila TRIM-NHL RNA-binding protein (RBP), MEI-P26, has previously been shown to suppress tumor formation in the germline. Here we show that, in the Drosophila larval central brain, cell-type specific expression of MEI-P26 plays a vital role in regulating neural development. MEI-P26 and another TRIM-NHL RBP, Brain tumor (BRAT), have distinct expression patterns in Type I neuroblast (NB) lineages: While both proteins are expressed in NBs, BRAT is expressed in ganglion mother cells (GMCs) but not neurons whereas MEI-P26 is expressed in neurons but not GMCs.
View Article and Find Full Text PDFIt is established that BCG vaccination results in the development of both a specific immune response to mycobacterial infections and a nonspecific (heterologous) immune response, designated as trained immunity (TRIM), to other pathogens. We hypothesized that local BCG immunization may induce an early immune response in bone marrow and spleen innate immunity cells. The early transcriptomic response of various populations of innate immune cells, including monocytes, neutrophils, and natural killer (NK) cells, to BCG vaccination was examined.
View Article and Find Full Text PDFGenes (Basel)
November 2024
Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 518 Ziyue Road, Shanghai 200241, China.
(TRIM26) is an E3 ubiquitin ligase and a member of the TRIM family. Similar to other TRIM proteins, TRIM26 consists of three domains, collectively termed RBCC: a Really Interesting New Gene (RING) domain, one B-Box domain, and a C terminal domain consisting of a PRY/SPRY domain. The PRY/SPRY domain exhibits relatively higher conservation compared with the RING and B-Box domains, suggesting potentially similar roles across TRIM26 proteins from various species.
View Article and Find Full Text PDFBMC Med Genomics
November 2024
University of East Anglia, Norwich, Norfolk, UK.
Cell Rep
December 2024
Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Pathology, Molecular, and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; The Icahn Genomics Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address:
Viral infection triggers a rapid and effective cellular response primarily mediated by interferon β (IFNβ), which induces an antiviral state through complex signaling cascades. To maintain a robust antiviral response while preventing excessive activation, the induction of IFNβ and downstream signaling are tightly regulated. Members of the tripartite-motif (TRIM) family of E3 ubiquitin (Ub) ligases play crucial roles in modulating these processes.
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