Over-expression of tobacco UBC1 encoding a ubiquitin-conjugating enzyme increases cadmium tolerance by activating the 20S/26S proteasome and by decreasing Cd accumulation and oxidative stress in tobacco (Nicotiana tabacum)

2017 ◽  
Vol 94 (4-5) ◽  
pp. 433-451 ◽  
Author(s):  
Ramin Bahmani ◽  
DongGwan Kim ◽  
Byoung Doo Lee ◽  
Seongbin Hwang
2021 ◽  
Author(s):  
Shahan Mamoor

Gynecologic cancers including cancers of the endometrium are a clinical problem (1-4). We mined published microarray data (5, 6) to discover genes associated with endometrial cancers by comparing transcriptomes of the normal endometrium and endometrial tumors from humans. We identified ubiquitin conjugating enzyme E2 C, encoded by UBE2C, as among the most differentially expressed genes, transcriptome-wide, in cancers of the endometrium. UBE2C was expressed at significantly higher levels in endometrial tumor tissues as compared to the endometrium. Importantly, primary tumor expression of UBE2C was correlated with overall survival in patients with endometrial cancer. UBE2C may be a molecule of interest in understanding the etiology or progression of human endometrial cancer.


2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Hongjie Yuan ◽  
Shibin Du ◽  
Youliang Deng ◽  
Xiaoqing Xu ◽  
Qian Zhang ◽  
...  

Abstract Background: MicroRNA can regulate gene expression, and participate in multiple vital activities, such as inflammation, oxidative stress epigenetic modification, cell proliferation, and apoptosis. It plays an important role in the genesis and development of cardiovascular disease. Objective: To assess the role of microRNA-208a in ketamine-induced cardiotoxicity. Methods: All rats were randomly selected into two groups: sham and model groups. After fixed, all rats in the model group was intraperitoneally (IP) injected with 100 mg/kg of ketamine. Heart samples were stained with HE assay. Total RNAs from serum were used to hybridize with the SurePrint G3 Rat Whole Genome GE 8×60 K Microarray G4858A platform. Results: In the rat model with ketamine-induced cardiotoxicity, microRNA-208a expression was increased. Then, over-expression of microRNA-208a increased inflammation and oxidative stress in vitro model. However, down-regulation of microRNA-208a decreased inflammation and oxidative stress in vitro model. Over-expression of microRNA-208a suppressed CHD9 and Notch1, and induced p65 protein expression in vitro model. Overexpression of CHD9 reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through Notch/p65 signal pathways. Notch1 activation reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through p65 signal pathways. Conclusion: MicroRNA-208a may be a potential biomarker for ketamine-induced cardiotoxicity through inflammation and oxidative stress by Notch/NF-κB signal pathways by CHD9.


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