{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5(11)"],"submitter":["Popova TG"],"pubmed_abstract":["Rift valley fever virus (RVFV) infection is an emerging zoonotic disease endemic in many countries of sub-Saharan Africa and in Egypt. In this study we show that human small airway epithelial cells are highly susceptible to RVFV virulent strain ZH-501 and the attenuated strain MP-12. We used the reverse-phase protein arrays technology to identify phosphoprotein signaling pathways modulated during infection of cultured airway epithelium. ZH-501 infection induced activation of MAP kinases (p38, JNK and ERK) and downstream transcriptional factors [STAT1 (Y701), ATF2 (T69/71), MSK1 (S360) and CREB (S133)]. NF-κB phosphorylation was also increased. Activation of p53 (S15, S46) correlated with the increased levels of cleaved effector caspase-3, -6 and -7, indicating activation of the extrinsic a"],"journal":["PloS one"],"pagination":["e13805"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2972203"],"repository":["biostudies-literature"],"pubmed_title":["Reverse-phase phosphoproteome analysis of signaling pathways induced by Rift valley fever virus in human small airway epithelial cells."],"pmcid":["PMC2972203"],"pubmed_authors":["Liotta L","Bailey C","Narayanan A","Kashanchi F","Kehn-Hall K","Espina V","Turell MJ","Kidd J","Petricoin EF","Popova TG","Popov SG"],"additional_accession":[]},"is_claimable":false,"name":"Reverse-phase phosphoproteome analysis of signaling pathways induced by Rift valley fever virus in human small airway epithelial cells.","description":"Rift valley fever virus (RVFV) infection is an emerging zoonotic disease endemic in many countries of sub-Saharan Africa and in Egypt. In this study we show that human small airway epithelial cells are highly susceptible to RVFV virulent strain ZH-501 and the attenuated strain MP-12. We used the reverse-phase protein arrays technology to identify phosphoprotein signaling pathways modulated during infection of cultured airway epithelium. ZH-501 infection induced activation of MAP kinases (p38, JNK and ERK) and downstream transcriptional factors [STAT1 (Y701), ATF2 (T69/71), MSK1 (S360) and CREB (S133)]. NF-κB phosphorylation was also increased. Activation of p53 (S15, S46) correlated with the increased levels of cleaved effector caspase-3, -6 and -7, indicating activation of the extrinsic a","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Nov","modification":"2025-04-04T21:04:39.141Z","creation":"2019-03-26T23:09:05Z"},"accession":"S-EPMC2972203","cross_references":{"pubmed":["21072193"],"doi":["10.1371/journal.pone.0013805"]}}