| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1963522 | Cellular Signalling | 2013 | 8 Pages |
Abstract
⺠Forskolin-induced cyclic AMP production was increased by knockdown of 4.1G. ⺠Forskolin-induced cAMP production was suppressed by overexpression of 4.1G. ⺠4.1G distributed on plasma membrane was crucial for the reduction of cAMP production. ⺠G protein-coupled receptor-mediated cAMP production was also modulated by 4.1G. ⺠4.1G regulates GPCR signals by suppressing adenylyl cyclase-mediated cAMP production.
Keywords
PTHRGPCR kinaseRGSGPCRFERMpKaEpacGRKPDECTDAGSERKEMEMHRPpTHHEKDMEMIBMX3-isobutyl-1-methylxanthinecyclic AMPcAMPDulbecco's modified Eagle's mediumSmall interfering RNAsiRNACyclic adenosine monophosphateAdenylyl cyclasesEagle's minimum essential mediumcarboxy-terminal domainPhosphodiesterasehemagglutininparathyroid hormoneHorseradish peroxidaseProtein 4.1exchange protein activated by cAMPprotein kinase Ahuman embryonic kidneyextracellular signal-regulated kinaseparathyroid hormone receptorG protein-coupled receptor
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Authors
Toshihiro Goto, Ayano Chiba, Jun Sukegawa, Teruyuki Yanagisawa, Masaki Saito, Norimichi Nakahata,