Viroids are small non-capsidated non-coding RNA replicons that utilize host factors for efficient propagation and spread through the entire plant. They can incite specific disease symptoms in susceptible plants. To better understand viroid-plant interactions, we employed microarray analysis to observe the changes of gene expression in "Rutgers" tomato leaves in response to the mild (M) and severe (S23) variants of potato spindle tuber viroid (PSTVd). The changes were analyzed over a time course of viroid infection development: (i) the pre-symptomatic stage; (ii) early symptoms; (iii) full spectrum of symptoms and (iv) the so-called 'recovery' stage, when stem regrowth was observed in severely affected plants. Gene expression profiles differed depending on stage of infection and variant. In S23-infected plants, the expression of over 3000 genes was affected, while M-infected plants showed 3-fold fewer differentially expressed genes, only 20% of which were specific to the M variant. The differentially expressed genes included many genes related to stress; defense; hormone metabolism and signaling; photosynthesis and chloroplasts; cell wall; RNA regulation, processing and binding; protein metabolism and modification and others. The expression levels of several genes were confirmed by nCounter analysis.
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http://dx.doi.org/10.3390/v10050257 | DOI Listing |
Chem Biodivers
January 2025
Biruni Universitesi, Molecular Biology and Genetics, Biruni Uni, İstanbul, TURKEY.
Regulation of protein production in response to physiological signals is achieved through precise control of Eukaryotic Elongation Factor 2 (eEF2), whose distinct translocase function is crucial for cell survival. Phosphorylation of eEF2 at its Thr56 (T56) residue inactivates this function in translation. Using genetically modified paralogue of a colon cancer cell line, HCT116 which carries a point mutation at Ser595-to-Alanine in the eEF2 gene we were able to create a constitutively active form of eEF2.
View Article and Find Full Text PDFJ Mol Cell Cardiol Plus
September 2024
National Research Center for Preventive Medicine (NRCPM), Petroverigsky, 10, building 3, Moscow 101990, Russia.
Background And Aims: Cadherins are adhesion proteins, and their dysregulation may result in the development of atherosclerosis, plaque rupture, or lesions of the vascular wall. The aim of the present study was to detect the associations of cadherins-P, -E, and -H, with atherosclerosis and pathological cardiovascular conditions.
Methods And Results: The present study with 3-year follow up evaluated atherosclerosis and fasting levels of P-, E-, and H-cadherins in the serum samples of 214 patients in a hospital setting.
J Mol Cell Cardiol Plus
March 2024
National Coalition of Independent Scholars, 125 Putney Road, Battleboro, VT 05301, United States.
Existing cardiovascular studies tend to suffer from small sample sizes and unaddressed confounders. Re-profiling of 9 microarray datasets revealed significant global gene expression differences between 358 failing and 191 non-failing left ventricles independent of age and sex ( = 5.1e-10).
View Article and Find Full Text PDFPeerJ
January 2025
Department of Endocrinology, Sir Run Run Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Purpose: In this study, we aimed to study the role of extracellular proteins as biomarkers associated with newly diagnosed Type 1 diabetes (NT1D) diagnosis and prognosis.
Patients And Methods: We retrieved and analyzed the GSE55098 microarray dataset from the Gene Expression Omnibus (GEO) database. Using R software, we screened out the extracellular protein-differentially expressed genes (EP-DEGs) through several protein-related databases.
Hellenic J Cardiol
January 2025
Department of Cardiac Surgery Research, Lankenau Institute for Medical Research, Main Line Health, Wynnewood, PA, 19096, USA; Department of Cardiac Surgery, Lankenau Heart Institute, Main Line Health, Wynnewood, PA, 19096, USA. Electronic address:
Objective: Thoracic Aortic Aneurysm (TAA) represents an aortic pathology that is caused by the deranged integrity of the three layers of the aortic wall, and is related to severe morbidity and mortality. Consequently, it is crucial to identify the biomarkers implicated in the pathogenesis and biology of TAA. The aim of the current computational study was to assess the differential gene expression profile of the gap junction proteins (GJPs) in patients with TAA in order to identify novel potential biomarkers for the diagnosis and treatment of this disease.
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