{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["16(6)"],"submitter":["Yulia A"],"funding":["Action Medical Research","Borne","National Institute for Health Research Biomedical Research Centre"],"pubmed_abstract":["Previously, we showed that cAMP increased COX-2 expression in myometrial cells via MAPK. Here, we have extended these observations, using primary myometrial cell cultures to show that the cAMP agonist, forskolin, enhances IL-1β-driven COX-2 expression. We then explored the role of A-kinase interacting protein (AKIP1), which modulates the effect of PKA on p65 activation. AKIP1 knockdown reversed the effect of forskolin, such that its addition inhibited IL-1β-induced COX-2 mRNA expression and reduced the IL-1β-induced increase in nuclear levels of p65 and c-jun. Forskolin alone and with IL-1β increased IκBα mRNA expression suggesting that in the context of inflammation and in the presence of AKIP1, cAMP enhances p65 activation. AKIP1 knockdown reversed these changes. Interestingly, AKIP1 kno"],"journal":["PloS one"],"pagination":["e0252720"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8224895"],"repository":["biostudies-literature"],"pubmed_title":["PKA and AKIP1 interact to mediate cAMP-driven COX-2 expression: A potentially pivotal interaction in preterm and term labour."],"pmcid":["PMC8224895"],"pubmed_authors":["Johnson MR","Lei K","Singh N","Varley AJ","Sooranna SR","Yulia A","Markovic D"],"additional_accession":[]},"is_claimable":false,"name":"PKA and AKIP1 interact to mediate cAMP-driven COX-2 expression: A potentially pivotal interaction in preterm and term labour.","description":"Previously, we showed that cAMP increased COX-2 expression in myometrial cells via MAPK. Here, we have extended these observations, using primary myometrial cell cultures to show that the cAMP agonist, forskolin, enhances IL-1β-driven COX-2 expression. We then explored the role of A-kinase interacting protein (AKIP1), which modulates the effect of PKA on p65 activation. AKIP1 knockdown reversed the effect of forskolin, such that its addition inhibited IL-1β-induced COX-2 mRNA expression and reduced the IL-1β-induced increase in nuclear levels of p65 and c-jun. Forskolin alone and with IL-1β increased IκBα mRNA expression suggesting that in the context of inflammation and in the presence of AKIP1, cAMP enhances p65 activation. AKIP1 knockdown reversed these changes. Interestingly, AKIP1 kno","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021","modification":"2026-05-08T00:24:38.791Z","creation":"2022-02-10T21:17:25.138Z"},"accession":"S-EPMC8224895","cross_references":{"pubmed":["34166397"],"doi":["10.1371/journal.pone.0252720"]}}