scholarly journals Iron-responsive element-binding protein. Phosphorylation by protein kinase C.

1993 ◽  
Vol 268 (36) ◽  
pp. 27363-27370
Author(s):  
R S Eisenstein ◽  
P T Tuazon ◽  
K L Schalinske ◽  
S A Anderson ◽  
J A Traugh
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Phosphorylation ◽  
Binding Protein ◽  
Iron Responsive Element ◽  
Kinase C ◽  
Element Binding Protein ◽  
Responsive Element

ROLE OF CAMP-RESPONSE ELEMENT-BINDING PROTEIN PHOSPHORYLATION IN HEPATIC APOPTOSIS UNDER PROTEIN KINASE C ?? SUPPRESSION DURING SEPSIS

Shock ◽  
2005 ◽  
Vol 24 (4) ◽  
pp. 357-363 ◽  
Author(s):  
Ya-Ching Hsieh ◽  
Yen-Hsu Chen ◽  
Hsiao-Ching Jao ◽  
Hseng-Kuang Hsu ◽  
Li-Ju Huang ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Phosphorylation ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Kinase C ◽  
Element Binding Protein

scholarly journals Chronic Gonadotropin-Releasing Hormone Inhibits Activin Induction of the Ovine Follicle-Stimulating Hormone β-Subunit: Involvement of 3′,5′-Cyclic Adenosine Monophosphate Response Element Binding Protein and Nitric Oxide Synthase Type I

Endocrinology ◽  
2007 ◽  
Vol 148 (7) ◽  
pp. 3346-3355 ◽  
Author(s):  
Farideh Shafiee-Kermani ◽  
Sang-oh Han ◽  
William L. Miller
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Binding Protein ◽  
Adenosine Monophosphate ◽  
Luciferase Expression ◽  
Type I ◽  
Response Element ◽  
Kinase C ◽  
Element Binding Protein

FSH is induced by activin, and this expression is modulated by GnRH through FSHB expression. This report focuses on the inhibitory effect of GnRH on activin-induced FSHB expression. Activin-treated primary murine pituitary cultures robustly express mutant ovine FSHBLuc-ΔAP1, a luciferase transgene driven by 4.7 kb of ovine FSHB promoter. This promoter lacks two GnRH-inducible activator protein-1 sites, making it easier to observe GnRH-mediated inhibition. Luciferase expression from this transgene was decreased 94% by 100 nm GnRH with a half-time of approximately 4 h in pituitary cultures, and this inhibition was independent of follistatin. Activators of cAMP and protein kinase C like forskolin and phorbol 12-myristate 3-acetate (PMA), respectively, mimicked GnRH action. Kinetic studies of wild-type ovine FSHBLuc in LβT2 cells showed continuous induction by activin (4-fold) over 20 h. Most of this induction (78%) was blocked, beginning at 6 h. cAMP response element binding protein (CREB) was implicated in this inhibition because overexpression of its constitutively active mutant mimicked GnRH, and its inhibitor (inducible cAMP early repressor isoform II) reversed the inhibition caused by GnRH, forskolin, or PMA. In addition, GnRH, forskolin, or PMA increased the expression of a CREB-responsive reporter gene, 6xCRE-37PRL-Luc. Inhibition of nitric oxide type I (NOSI) by 7-nitroindazole also reversed GnRH-mediated inhibition by 60%. It is known that GnRH and CREB induce production of NOSI in gonadotropes and neuronal cells, respectively. These data support the concept that chronic GnRH inhibits activin-induced ovine FSHB expression by sequential activation of CREB and NOSI through the cAMP and/or protein kinase C pathways.

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