scholarly journals Protein kinase A inhibition of macrophage maturation is accompanied by an increase in DNA methylation of the colony-stimulating factor 1 receptor gene

Immunology ◽  
2016 ◽  
Vol 149 (2) ◽  
pp. 225-237 ◽  
Author(s):  
Zbigniew Zasłona ◽  
Anne M. Scruggs ◽  
Marc Peters-Golden ◽  
Steven K. Huang
Keyword(s):  
Dna Methylation ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Receptor Gene ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Kinase A

Interactions Between the Inositol 1,4,5-Trisphosphate and Cyclic AMP Signaling Pathways Regulate Larval Molting in Drosophila

Genetics ◽  
2001 ◽  
Vol 158 (1) ◽  
pp. 309-318 ◽  
Author(s):  
K Venkatesh ◽  
G Siddhartha ◽  
Rohit Joshi ◽  
Sonal Patel ◽  
Gaiti Hasan
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Signaling Pathways ◽  
Feedback Inhibition ◽  
Receptor Gene ◽  
Dominant Negative ◽  
Neural Signals ◽  
Inositol 1,4,5 Trisphosphate ◽  
Kinase A ◽  
Insp3 Receptor

Abstract Larval molting in Drosophila, as in other insects, is initiated by the coordinated release of the steroid hormone ecdysone, in response to neural signals, at precise stages during development. In this study we have analyzed, using genetic and molecular methods, the roles played by two major signaling pathways in the regulation of larval molting in Drosophila. Previous studies have shown that mutants for the inositol 1,4,5-trisphosphate receptor gene (itpr) are larval lethals. In addition they exhibit delays in molting that can be rescued by exogenous feeding of 20-hydroxyecdysone. Here we show that mutants for adenylate cyclase (rut) synergize, during larval molting, with itpr mutant alleles, indicating that both cAMP and InsP3 signaling pathways function in this process. The two pathways act in parallel to affect molting, as judged by phenotypes obtained through expression of dominant negative and dominant active forms of protein kinase A (PKA) in tissues that normally express the InsP3 receptor. Furthermore, our studies predict the existence of feedback inhibition through protein kinase A on the InsP3 receptor by increased levels of 20-hydroxyecdysone.

scholarly journals Expression of the Mouse Gonadotropin-Releasing Hormone Receptor Gene in αT3-1 Gonadotrope Cells Is Stimulated by Cyclic 3′,5′-Adenosine Monophosphate and Protein Kinase A, and Is Modulated by Steroidogenic Factor-1 and Nur77

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 1958-1971 ◽  
Author(s):  
Hanél Sadie ◽  
Gustav Styger ◽  
Janet Hapgood
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Nuclear Receptor ◽  
Receptor Gene ◽  
Control Point ◽  
Negative Regulator ◽  
Mrna Levels ◽  
Orphan Nuclear Receptor ◽  
Steroidogenic Factor 1 ◽  
Kinase A

Regulation of GnRH receptor (GnRHR) expression levels in the pituitary is a crucial control point in reproduction. The promoter of the mouse GnRHR gene contains nuclear receptor half-sites (NRS) at –244/−236 and −15/−7 relative to the translation start site. Although binding of steroidogenic factor-1 (SF-1) to the –244/−236NRS is implicated in mediating basal and gonadotrope-specific expression, no function or protein-DNA interactions have previously been described for the –15/−7NRS. We report that levels of the endogenous GnRHR mRNA in αT3-1 cells are stimulated by forskolin and 8-bromo-cAMP. We also show that the orphan nuclear receptor Nur77 is expressed in αT3-1 cells, and that both SF-1 and Nur77 bind to the –15/−7NRS and –244/−236NRS in vitro. We show that the activity of the proximal (−579/+1) mouse GnRHR promoter is up-regulated by protein kinase A, via a mechanism that is modulated by SF-1, both positively and negatively, through binding to the –244/−236NRS or the –15/−7NRS, respectively. Nur77 appears to be capable of acting as a negative regulator of this response, via the –15/−7NRS. Furthermore, we show that forskolin up-regulates SF-1 mRNA levels in αT3-1 cells, indicating that the levels of SF-1 play a role in modulating the protein kinase A response.

scholarly journals Expression of Novel Neurotrophin-1/B-Cell Stimulating Factor-3 (NNT-1/BSF-3) in Murine Pituitary Folliculostellate TtT/GF Cells: Pituitary Adenylate Cyclase-Activating Polypeptide and Vasoactive Intestinal Peptide-Induced Stimulation of NNT-1/BSF-3 Is Mediated by Protein Kinase A, Protein Kinase C, and Extracellular-Signal-Regulated Kinase1/2 Pathways

Endocrinology ◽  
2004 ◽  
Vol 145 (2) ◽  
pp. 716-727 ◽  
Author(s):  
George Vlotides ◽  
Kathrin Zitzmann ◽  
Sabine Hengge ◽  
Dieter Engelhardt ◽  
Gunter K. Stalla ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Adenylate Cyclase ◽  
B Cell ◽  
Mrna Expression ◽  
Protein Kinase A ◽  
Kinase C ◽  
Pituitary Adenylate Cyclase ◽  
Stimulating Factor ◽  
Kinase A

Abstract Novel neurotrophin-1/B cell stimulating factor-3 (NNT-1/BSF-3) is a gp130 cytokine potently stimulating corticotroph proopiomelanocortin gene expression and ACTH secretion by a Janus kinase-signal transducer and activator of transcription (JAK-STAT)-dependent mechanism. In the current study, we examined the regulation of NNT-1/BSF-3 mRNA expression in murine pituitary folliculostellate TtT/GF cells using Northern blot technique. A 5- to 9-fold and a 4- to 7-fold induction in NNT-1/BSF-3 mRNA expression was observed between 2 and 6 h stimulation with the protein kinase C (PKC) stimulus phorbol-12-myristate-13-acetate (100 nm) and the protein kinase A (PKA) stimulus Bu2cAMP (5 mm), respectively. Pituitary adenylate cyclase-activating polypeptide (PACAP-38, 50 nm) and vasoactive intestinal peptide (VIP, 50 nm) also stimulated NNT-1/BSF-3 mRNA expression 5- to 9-fold between 2 and 6 h. Preincubation with PKC and PKA inhibitors such as H-7 (20 μm), GF109203X (50 μm), and H-89 (50 μm) decreased the stimulatory effects of PACAP and VIP. Both PACAP-38 and VIP also rapidly induced ERK1/2 phosphorylation and their stimulatory effect on NNT-1/BSF-3 mRNA expression was reduced by the MAPK kinase/ERK kinase (MEK) inhibitor U0126 (10 μm). Dexamethasone (10−7m) was a potent inhibitor of phorbol-12-myristate-13-acetate-induced NNT-1/BSF-3 expression. RT-PCR analysis demonstrated TtT/GF cells to express the short and the hop variant but not the hip variant of the PACAP-1 receptor (PAC1-R). In addition, TtT/GF cells express the VIP/PACAP-2 receptor (VPAC2-R). In summary, NNT-1/BSF-3 is expressed in pituitary folliculostellate TtT/GF cells and induced by PKC-, PKA-, and ERK1/2-dependent mechanisms. The novel gp130 cytokine NNT-1/BSF-3 derived from folliculostellate cells might act as a paracrine neuroimmunoendocrine modulator of pituitary corticotroph function.

Sign in / Sign up

Export Citation Format

Share Document