scholarly journals Prognostic impact of AMP-activated protein kinase expression in ovarian carcinoma: Correlation of protein expression and GC/TOF-MS-based metabolomics

2011 ◽  
Vol 25 (4) ◽  
Author(s):  
Denkert
PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0119680 ◽  
Author(s):  
Michael J. Bertoldo ◽  
Edith Guibert ◽  
Melanie Faure ◽  
Christelle Ramé ◽  
Marc Foretz ◽  
...  

2017 ◽  
Vol 292 (21) ◽  
pp. 8716-8728 ◽  
Author(s):  
Yoshifumi Sato ◽  
Tomonori Tsuyama ◽  
Chinami Sato ◽  
Md. Fazlul Karim ◽  
Tatsuya Yoshizawa ◽  
...  

2012 ◽  
Vol 23 (1) ◽  
pp. 78-85 ◽  
Author(s):  
W.N. William ◽  
J.-S. Kim ◽  
D.D. Liu ◽  
L. Solis ◽  
C. Behrens ◽  
...  

2008 ◽  
Vol 295 (4) ◽  
pp. E938-E946 ◽  
Author(s):  
Hui Sheng ◽  
Tingting Sun ◽  
Binhai Cong ◽  
Ping He ◽  
Yanmin Zhang ◽  
...  

Corticotropin-releasing hormone (CRH) has been shown to exhibit various functions in hippocampus. In the present study, we examined the effect of CRH on the expression of serum/glucocorticoid-inducible protein kinase-1 (SGK-1), a novel protein kinase, in primary cultured hippocampal neurons. A dose-dependent increase in mRNA and protein levels of SGK-1 as well as frequency of SGK-1-positive neurons occurred upon exposure to CRH (1 pmol/l to 10 nmol/l). These effects can be reversed by the specific CRH-R1 antagonist antalarmin but not by the CRH-R2 antagonist astressin 2B. Blocking adenylate cyclase (AC) activity with SQ22536 and PKA with H89 completely prevented CRH-induced mRNA and protein expression of SGK-1. Blockage of PLC or PKC did not block CRH-induced SGK-1 expression. Our results suggest that CRH act on CRH-R1 to stimulate SGK-1 mRNA and protein expression in cultured hippocampal neurons via a mechanism that is involved in AC/PKA signaling pathways.


2013 ◽  
Vol 91 (12) ◽  
pp. 1025-1030 ◽  
Author(s):  
Saadet Turkseven ◽  
Elif Ertuna

AMP-activated protein kinase (AMPK) is a regulator of cellular metabolism and is involved in the pathogenesis of several diseases, including type 2 diabetes and cardiovascular diseases. Data showing the effects of AMPK on vasculature are controversial. Therefore, the aim of this study was to determine the impact of prolonged AMPK activation on vascular functions. For this purpose we have examined the role of AMPK in endothelium-dependent and -independent relaxation and vascular contractions. For this, we incubated thoracic aortic rings, from rats, with AMPK activator 5-aminoimidazole-4-carboxamide-1-4-ribofuranoside (AICAR, 500 μmol/L or 2 mmol/L) in the presence or absence of AMPK inhibitor compound C (10 μmol/L). Next, cumulative dose–response curves to acetylcholine (ACh) (10−9−10−4 mol/L), nitroglycerine (NG) (10−9–3 × 10−5 mol/L), and noradrenaline (NA) (10−9−10−4 mol/L) were obtained. Endothelial nitric oxide synthase (eNOS) protein expression was determined. Our results show that endothelium-dependent relaxation was inhibited after AICAR treatment, and that this effect was reversed by AMPK inhibition. Moreover, AICAR enhanced the contractile response to NA and caused a decrease in eNOS protein expression. In conclusion, prolonged AMPK induction causes endothelial impairment, possibly via increased degradation and (or) reduced expression of eNOS.


Oncology ◽  
2011 ◽  
Vol 80 (1-2) ◽  
pp. 130-134 ◽  
Author(s):  
Akin Atmaca ◽  
Claudia Pauligk ◽  
Kristina Steinmetz ◽  
Hans-Michael Altmannsberger ◽  
Elke Jäger ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document