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https://scholarbank.nus.edu.sg/handle/10635/137981
DC Field | Value | |
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dc.title | RESPIRABLE SIRNA TARGETING AT THE NF-KB PATHWAY PROTECTS AGAINST INFLAMMATORY LUNG DISEASES | |
dc.contributor.author | DONG JINRUI | |
dc.date.accessioned | 2017-12-18T18:00:18Z | |
dc.date.available | 2017-12-18T18:00:18Z | |
dc.date.issued | 2017-08-04 | |
dc.identifier.citation | DONG JINRUI (2017-08-04). RESPIRABLE SIRNA TARGETING AT THE NF-KB PATHWAY PROTECTS AGAINST INFLAMMATORY LUNG DISEASES. ScholarBank@NUS Repository. | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/137981 | |
dc.description.abstract | Asthma and chronic obstructive pulmonary disease (COPD) are common inflammatory pulmonary diseases. Cumulative evidences have shown the role of NF-kB signaling pathway in the pathogenesis of asthma and COPD. Ribosomal protein S3 (RPS3) is a subunit of NF-kB complex while receptor-interacting protein 2 (Rip2) is a positive upstream regulator of NF-kB pathway. In my PhD projects, I sought to investigate if RPS3 and Rip2 siRNA could protect against HDM-induced mouse asthma model or CS-induced mouse COPD model. RPS3 and Rip2 siRNA markedly knocked down RPS3 and Rip2 levels in mouse cell lines and mouse lung. RPS3 siRNA abated HDM-induced mucus hypersecretion, cytokine production, and serum IgE elevation. RPS3 and Rip2 siRNA ameliorated neutrophil infiltration and suppressed CS-induced inflammatory and oxidative damage marker levels. Here we reported that RPS3 and Rip2 siRNA ameliorated lung inflammation via the interruption of NF-kB activity, postulating the therapeutic potential of them. | |
dc.language.iso | en | |
dc.subject | Asthma, COPD, NF-kB, RPS3, Rip2 | |
dc.type | Thesis | |
dc.contributor.department | PHARMACOLOGY | |
dc.contributor.supervisor | WONG WAI-SHIU, FRED | |
dc.description.degree | Ph.D | |
dc.description.degreeconferred | DOCTOR OF PHILOSOPHY | |
Appears in Collections: | Ph.D Theses (Open) |
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DongJR.pdf | 4.64 MB | Adobe PDF | OPEN | None | View/Download |
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