Proteomic analysis identifies prohibitin down-regulation as a crucial event in the mitochondrial damage observed in HIV-infected patients

2010 ◽  
Vol 15 (3) ◽  
pp. 377-390 ◽  
Author(s):  
Fabiola Ciccosanti ◽  
Marco Corazzari ◽  
Fabio Soldani ◽  
Paola Matarrese ◽  
Vittoria Pagliarini ◽  
...  
PROTEOMICS ◽  
2010 ◽  
Vol 10 (7) ◽  
pp. 1474-1483 ◽  
Author(s):  
Shufang Liang ◽  
Afu Fu ◽  
Qiang Zhang ◽  
Minghai Tang ◽  
Jin Zhou ◽  
...  

2009 ◽  
Vol 8 (8) ◽  
pp. 4050-4061 ◽  
Author(s):  
James D. Bortner ◽  
Arunangshu Das ◽  
Todd M. Umstead ◽  
Williard M. Freeman ◽  
Richard Somiari ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Bao-hua Dong ◽  
Zhao-qing Niu ◽  
Jing-tao Zhang ◽  
Yi-jing Zhou ◽  
Fan-mei Meng ◽  
...  

Parkinson’s disease (PD) is a disease that involves brain damage and is associated with neuroinflammation, mitochondrial damage, and cell aging. However, the pathogenic mechanism of PD is still unknown. Sequencing data and proteomic data can describe the fluctuation of molecular abundance in diseases at the mRNA level and protein level, respectively. In order to explore new targets in the pathogenesis of PD, the study analyzed molecular changes from the database by combining transcriptomic and proteomic analysis. Differentially expressed genes and differentially abundant proteins were summarized and analyzed. Enrichment and cluster analysis emphasized the importance of neurotransmitter release, mitochondrial damage, and vesicle transport. The molecular network revealed a subnetwork of 9 molecules related to SCNA and TH and revealed hub gene with differential expression at both mRNA and protein levels. It found that ACHE and CADPS could be used as new targets in PD, emphasizing that impaired nerve signal transmission and vesicle transport affect the pathogenesis of PD. Our research emphasized that the joint analysis and verification of transcriptomics and proteomics were devoted to understanding the comprehensive views and mechanism of pathogenesis in PD.


2008 ◽  
Vol 35 (5) ◽  
pp. 360 ◽  
Author(s):  
Poonam Bhargava ◽  
Arvind Kumar ◽  
Yogesh Mishra ◽  
Lal Chand Rai

This study provides first-hand proteomic characterisation of Cu-pretreatment-induced augmentation of ultraviolet B toxicity in the cyanobacterium Anabaena doliolum Bharadwaja. Of the three treatments (i.e. Cu, UV-B and Cu + UV-B) tested, the UV-B treatment of Cu-pretreated Anabaena produced a greater inhibition of oxygen evolution, 14C fixation, ATP and NADPH contents than UV-B alone. Proteomic analysis using two-dimensional gel electrophoresis (2DE), MALDI-TOF MS/MS and reverse transcription polymerase chain reaction (RT–PCR) of Cu, UV-B, and Cu + UV-B treated Anabaena exhibited significant and reproducible alterations in 12 proteins. Of these, manganese superoxide dismutase (Mn-SOD), iron superoxide dismutase (Fe-SOD) and peroxiredoxin (PER) are antioxidative enzymes; ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCo), phosphoribulokinase (PRK), flavodoxin (Flv), plastocyanin (PLC), phosphoglycerate kinase (PGK), phycocyanin (PC) and phycoerythrocyanin α-chain (PC α-chain) are linked with photosynthesis and respiration; and DnaK and nucleoside diphosphate kinase (NDPK) are associated with cellular processes and light signalling, respectively. However, when subjected to a high dose of UV-B, Cu-pretreated Anabaena depicted a severe down-regulation of DnaK, NDPK and Flv, probably because of inevitable oxidative stress. Thus, the augmentation of UV-B toxicity by Cu can be attributed to the down-regulation of DnaK, NDPK and Flv.


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