scholarly journals Co-localization and confinement of ecto-nucleotidases modulate extracellular adenosine nucleotide distributions

2020 ◽  
Vol 16 (6) ◽  
pp. e1007903 ◽  
Author(s):  
Hadi Rahmaninejad ◽  
Tom Pace ◽  
Shashank Bhatt ◽  
Bin Sun ◽  
Peter Kekenes-Huskey
1995 ◽  
Vol 32 (8) ◽  
pp. 221-225 ◽  
Author(s):  
M. Greetham ◽  
B. Holden ◽  
J. Scutt

Analysis of the biofilm on a distribution system model pipe rig gave high readings of extracellular adenosine-5′-triphosphate (ATP). The free ATP was assumed to come from dead cells at the base of the biofilm. The levels were large in proportion to the measured cellular ATP and were unstable. This resulted in errors in the calculation of cellular ATP. An enzyme Somase (0.5%) was employed to hydrolyse the free ATP. Increased accuracy of the measurement of cellular ATP was seen.


2019 ◽  
Vol 19 (16) ◽  
pp. 1445-1463 ◽  
Author(s):  
Jindian Li ◽  
Xingfang Hong ◽  
Guoquan Li ◽  
Peter S. Conti ◽  
Xianzhong Zhang ◽  
...  

Adenosine receptors (ARs) are a class of purinergic G-protein-coupled receptors (GPCRs). Extracellular adenosine is a pivotal regulation molecule that adjusts physiological function through the interaction with four ARs: A1R, A2AR, A2BR, and A3R. Alterations of ARs function and expression have been studied in neurological diseases (epilepsy, Alzheimer’s disease, and Parkinson’s disease), cardiovascular diseases, cancer, and inflammation and autoimmune diseases. A series of Positron Emission Tomography (PET) probes for imaging ARs have been developed. The PET imaging probes have provided valuable information for diagnosis and therapy of diseases related to alterations of ARs expression. This review presents a concise overview of various ARs-targeted radioligands for PET imaging in diseases. The most recent advances in PET imaging studies by using ARs-targeted probes are briefly summarized.


1988 ◽  
Vol 263 (25) ◽  
pp. 12367-12372
Author(s):  
G A Weisman ◽  
K D Lustig ◽  
E Lane ◽  
N N Huang ◽  
I Belzer ◽  
...  

Islets ◽  
2012 ◽  
Vol 4 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Gary K. Yang ◽  
Paul E. Squires ◽  
Faming Tian ◽  
Timothy J. Kieffer ◽  
Yin Nam Kwok ◽  
...  

PROTEOMICS ◽  
2010 ◽  
Vol 10 (2) ◽  
pp. 235-244 ◽  
Author(s):  
Stephen Chivasa ◽  
William J. Simon ◽  
Alex M. Murphy ◽  
Keith Lindsey ◽  
John P. Carr ◽  
...  

1982 ◽  
Vol 60 (3) ◽  
pp. 302-307 ◽  
Author(s):  
M. J. York ◽  
L. P. Davies

We have used the adenosine-stimulated adenylate cyclase of guinea-pig brain to examine the potency of diazepam as an adenosine uptake inhibitor. Diazepam at concentrations in the range 10–500 μM stimulates the production of cAMP in incubated slices of guinea-pig cerebral cortex, with maximal fivefold stimulations over basal levels by 200 μM diazepam. The increases can be largely (but not completely) blocked by the adenosine antagonist theophylline or by addition of excess adenosine deaminase to the system. It appears that the stimulation of cAMP production is due to a blockade of adenosine uptake which results in an increase in extracellular adenosine and concomitant activation of the adenosine receptor coupled to adenylate cyclase. Since the cAMP response to standard adenosine uptake blockers (dipyridamole, dilazep) can be completely blocked by theophylline or adenosine deaminase, a small component of the diazepam response cannot be explained by an adenosine effect. The concentration of diazepam at which the first significant cAMP increase occurs is 10 μM or slightly lower. This is significantly higher than the concentration of diazepam needed to saturate the pharmacologically characterized central nervous system receptors for benzodiazepines.


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