Retinoic acid-induced human secretin gene expression in neuronal cells is mediated by cyclin-dependent kinase 1.
Previously, we found that secretin transcript levels were induced by all-trans retinoic acid (RA) in a neuroblastoma cell model, SH-SY5Y. In this article, this RA-dependent upregulation process was further investigated. In the cyclin-dependent kinase 1 (Cdk1) inhibitor-treated cells, the RA-dependent induction of secretin gene expression was inhibited. Together with our previous works, we propose here that the RA responsiveness of the secretin promotor is mediated by two different pathways. The first pathway is by changing the expression levels of NFI-C and Sp proteins while the second pathway is by modifying the phosphorylation status of both NFI-C and Sp proteins via Cdk1.
Lee
Leo T O
LT
Department of Zoology, The University of Hong Kong, Pokfulam Road, Hong Kong, PRC.
Tan-Un
K C
KC
Chow
Billy K C
BK
D016203:CDC2 Protein Kinase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D045744:Cell Line, Tumor; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D009447:Neuroblastoma / Q000201:enzymology* / Q000235:genetics*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D012633:Secretin / Q000235:genetics*; D014212:Tretinoin / Q000494:pharmacology*
D047428:Protein Kinase Inhibitors; D012633:Secretin; D014212:Tretinoin; D016203:CDC2 Protein Kinase