Inhibition of prohormone convertase 1 (PC1) expression in cholecystokinin (CCK) expressing At-T20 cells decreased cellular content and secretion of CCK and caused a shift in molecular forms of CCK secreted.
Two different RNAi methods were used to inhibit the expression of prohormone convertase 1 (PC1) in At-T20 cells. Transient transfection of double stranded RNA and stable expression of a vector expressing hairpin-loop RNA targeting PC1 reduced cholecystokinin (CCK) secretion from At-T20 cells. PC1 mRNA and protein were also decreased in the vector transfected cells. This treatment caused a shift in the forms of cholecystokinin (CCK) secreted, decreasing CCK 22 and increasing CCK 8. Stable expression of RNAi effectively decreased PC1 expression. The observed decrease in CCK seen with these RNAi treatments further supports a role for PC1 in CCK processing in these cells.
Beinfeld
Margery C
MC
Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA.
Vishnuvardhan
Daesety
D
Blum
Alissa
A
Reynolds
Nicole
N
Fannous
Sanya
S
Kitagawa
Kouki
K
Marchand
James E
JE
D000595:Amino Acid Sequence; D000818:Animals; D002460:Cell Line; D002766:Cholecystokinin / Q000737:chemistry* / Q000378:metabolism*; D015870:Gene Expression / Q000187:drug effects; D051379:Mice; D008969:Molecular Sequence Data; D045664:Proprotein Convertase 1 / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics; D020033:Protein Isoforms / Q000737:chemistry / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats
D020033:Protein Isoforms; D012333:RNA, Messenger; D002766:Cholecystokinin; D045664:Proprotein Convertase 1