scholarly journals Human Osteocalcin and Bone Sialoprotein Mediating Osteomimicry of Prostate Cancer Cells: Role of cAMP-Dependent Protein Kinase A Signaling Pathway

2005 ◽  
Vol 65 (6) ◽  
pp. 2303-2313 ◽  
Author(s):  
Wen-Chin Huang ◽  
Zhihui Xie ◽  
Hiroyuki Konaka ◽  
Jaro Sodek ◽  
Haiyen E. Zhau ◽  
...  
2005 ◽  
Vol 117 (4) ◽  
pp. 551-560 ◽  
Author(s):  
Venkata S. Sabbisetti ◽  
Srinivasulu Chirugupati ◽  
Shibu Thomas ◽  
Kedar S. Vaidya ◽  
Dean Reardon ◽  
...  

2013 ◽  
Vol 228 (6) ◽  
pp. 1159-1165 ◽  
Author(s):  
Hyo-Kyoung Choi ◽  
Jung-Yoon Yoo ◽  
Mi-Hyeon Jeong ◽  
Soo-Yeon Park ◽  
Dong-Myoung Shin ◽  
...  

Cell Cycle ◽  
2014 ◽  
Vol 13 (20) ◽  
pp. 3292-3301 ◽  
Author(s):  
Evan R Zynda ◽  
Vitaliy Matveev ◽  
Michael Makhanov ◽  
Alexander Chenchik ◽  
Eugene S Kandel

1999 ◽  
Vol 276 (6) ◽  
pp. G1521-G1530 ◽  
Author(s):  
M. Kurjak ◽  
R. Fritsch ◽  
D. Saur ◽  
V. Schusdziarra ◽  
H. D. Allescher

The effect of nitric oxide (NO) on the release of bombesin-like immunoreactivity (BLI) was examined in synaptosomes of rat small intestine. The NO donor S-nitroso- N-acetylpenicillamine (SNAP; 10−7 to 10−4 M) significantly stimulated BLI release. In the presence of the NO scavenger oxyhemoglobin (10−3 M) or the guanylate cyclase inhibitor ODQ (10−5 M), SNAP-induced BLI release was antagonized. In addition, SNAP increased the synaptosomal cGMP content and elevation of cGMP levels by zaprinast (3 × 10−5 M), an inhibitor of the cGMP-specific phosphodiesterase (PDE) type 5, and increased basal and SNAP-induced BLI release. NO-induced BLI release was blocked by Rp-adenosine 3′,5′-cyclic monophosphorothioate (3 × 10−5 M and 10−4 M), an inhibitor of the cAMP-dependent protein kinase A, whereas KT-5823 (3 × 10−6 M) and Rp-8-(4-chlorophenylthio)-cGMP (5 × 10−5M), inhibitors of the cGMP-dependent protein kinase G, had no effect. Because cGMP inhibits the cAMP-specific PDE3, thereby increasing cAMP levels, the role of PDE3 was investigated. Trequinsin (10−8 M), a specific blocker of PDE3, stimulated basal BLI release but had no additive effect on NO-induced release, suggesting a similar mechanism of action. These data demonstrate that because of a cross-activation of cAMP-dependent protein kinase A by endogenous cGMP BLI can be released by NO from enteric synaptosomes.


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