Induction of Mx-related protein in cat peripheral blood mononuclear cells after administration of recombinant human interferon hybrid

1990 ◽  
Vol 13 (2) ◽  
pp. 53-59 ◽  
Author(s):  
M.A. Horisberger ◽  
R. Schrenk ◽  
S. Staiger ◽  
A.R. Leyvraz ◽  
S. Martinod
2020 ◽  
Author(s):  
Jyoti Kundu ◽  
Shikha Bakshi ◽  
Himanshu Joshi ◽  
Sanjay K Bhadada ◽  
Indu Verma ◽  
...  

AbstractBackgroundDiabetes is an important risk factor for developing tuberculosis. This association leads to exacerbation of tuberculosis symptoms and delayed treatment of both the diseases. Molecular mechanism and biomarkers/drug targets related to copathogenesis of tuberculosis and diabetes, however, still remains to be poorly understood. In this study, proteomics based 2D-MALDI/MS approach was employed to identify host signature proteins which are altered during copathogenesis of tuberculosis and diabetes.MethodsComparative proteome of human peripheral blood mononuclear cells (PBMCs) from healthy controls, tuberculosis and diabetes patients in comparison to comorbid diabetes and tuberculosis patients was analyzed. Gel based proteomics approach followed by in gel trypsin digestion and peptide identification by mass spectrometry was used for signature protein identification.ResultsTotal of 18 protein spots with differential expression in TBDM patients in comparison to other groups were identified. These include Vimentin, tubulin beta chain protein, superoxide dismutase, Actin related protein 2/3 complex subunit 2, PDZ LIM domain protein, Rho-GDP dissociation inhibitor, Ras related protein Rab, dCTPpyrophosphatase 1, Transcription initiation factor TFIID subunit 12, coffilin 1, three isoforms of Peptidylprolylcis-trans isomerase A, three isoforms of Protein S100A9, Protein S100A8 and SH3 domain containing protein. These proteins belonged to four functional categories i.e. structural, cell cycle/growth regulation, signaling and intermediary metabolism.ConclusionProteins identified to be differentially expressed in TBDM patient can act as potent biomarkers and as predictors for copathogenesis of tuberculosis and diabetes.


PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0233326
Author(s):  
Jyoti Kundu ◽  
Shikha Bakshi ◽  
Himanshu Joshi ◽  
Sanjay K. Bhadada ◽  
Indu Verma ◽  
...  

Background Diabetes is an important risk factor for developing tuberculosis. This association leads to exacerbation of tuberculosis symptoms and delayed treatment of both the diseases. Molecular mechanism and biomarkers/drug targets related to copathogenesis of tuberculosis and diabetes are still poorly understood. In this study, proteomics based 2D-MALDI/MS approach was employed to identify host signature proteins which are altered during copathogenesis of tuberculosis and diabetes. Methods Comparative proteome of human peripheral blood mononuclear cells (PBMCs) from healthy controls, tuberculosis and diabetes patients in comparison to comorbid diabetes and tuberculosis patients was analyzed. Gel based proteomics approach followed by in gel trypsin digestion and peptide identification by mass spectrometry was used for signature protein identification. Results Total of 18 protein spots with differential expression in tuberculosis and diabetes copathogenesis (TBDM) patients in comparison to other groups were identified. These proteins belonged to four functional categories i.e. structural, cell cycle/growth regulation, signaling and intermediary metabolism. These include Vimentin, tubulin beta chain protein, Actin related protein 2/3 complex subunit 2, coffilin 1 (Structural), PDZ LIM domain protein, Rho-GDP dissociation inhibitor, Ras related protein Rab (signaling), superoxide dismutase, dCTPpyrophosphatase 1, Transcription initiation factor TFIID subunit 12, three isoforms of Peptidylprolylcis-trans isomerase A, SH3 domain containing protein (metabolism), three isoforms of Protein S100A9 and S100A8 (cell cycle progression/growth regulation). Conclusion Proteins identified to be differentially expressed in TBDM patient can act as potent biomarkers and as predictors for copathogenesis of tuberculosis and diabetes.


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