Hydrophobic labeling of (sodium, potassium)-ATPase: further evidence that the .beta. subunit is embedded in the membrane bilayer

Biochemistry ◽  
1983 ◽  
Vol 22 (9) ◽  
pp. 2296-2300 ◽  
Author(s):  
M. Girardet ◽  
K. Geering ◽  
B. C. Rossier ◽  
J. P. Kraehenbuhl ◽  
C. Bron
Keyword(s):  
Beta Subunit ◽  
Membrane Bilayer ◽  
Sodium Potassium ◽  
Potassium Atpase

.beta. Subunit of sodium-potassium ATPase contains three disulfide bonds

Biochemistry ◽  
1990 ◽  
Vol 29 (6) ◽  
pp. 1524-1532 ◽  
Author(s):  
Richard P. Miller ◽  
Robert A. Farley
Keyword(s):  
Disulfide Bonds ◽  
Beta Subunit ◽  
Sodium Potassium ◽  
Potassium Atpase

Hydrophobic C-terminal amino acids in the .beta.-subunit are involved in assembly with the .alpha.-subunit of sodium-potassium-ATPase

Biochemistry ◽  
1993 ◽  
Vol 32 (51) ◽  
pp. 14117-14124 ◽  
Author(s):  
Ahmed T. Beggah ◽  
Pascal Beguin ◽  
Philippe Jaunin ◽  
Manuel C. Peitsch ◽  
Kaethi Geering
Keyword(s):  
Amino Acids ◽  
Beta Subunit ◽  
Alpha Subunit ◽  
Sodium Potassium ◽  
Terminal Amino ◽  
Potassium Atpase

Adenosine Receptor Modulation of Hypoxic-ischemic Injury in Striatum of Newborn Piglets

2020 ◽  
Vol 17 (4) ◽  
pp. 510-517
Author(s):  
Santiago Ortega-Gutierrez ◽  
Brandy Jones ◽  
Alan Mendez-Ruiz ◽  
Pankhil Shah ◽  
Michel T. Torbey
Keyword(s):  
Oxidative Stress ◽  
Atpase Activity ◽  
Neuronal Injury ◽  
Receptor Activation ◽  
Adult Mortality ◽  
Vehicle Group ◽  
Sodium Potassium ◽  
Receptor Modulation ◽  
A2a Receptor ◽  
Potassium Atpase

Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of pediatric and adult mortality and morbidity. Unfortunately, to date, no effective treatment has been identified. In the striatum, neuronal injury is analogous to the cellular mechanism of necrosis observed during NMethyl- D-Aspartate (NMDA) excitotoxicity. Adenosine acts as a neuromodulator in the central nervous system, the role of which relies mostly on controlling excitatory glutamatergic synapses. Objective: To examine the effect of pretreatment of SCH58261, an adenosine 2A (A2A) receptor antagonist and modulator of NMDA receptor function, following hypoxic-ischemia (HI) on sodium- potassium ATPase (Na+, K+-ATPase) activity and oxidative stress. Methods: Piglets (4-7 days old) were subjected to 30 min hypoxia and 7 min of airway occlusion producing asphyxic cardiac arrest. Groups were divided into four categories: HI samples were divided into HI-vehicle group (n = 5) and HI-A2A group (n = 5). Sham controls were divided into Sham vehicle (n = 5) and Sham A2A (n = 5) groups. Vehicle groups were pretreated with 0.9% saline, whereas A2A animals were pretreated with SCH58261 10 min prior to intervention. Striatum samples were collected 3 h post-arrest. Sodium-potassium ATPase (Na+, K+-ATPase) activity, malondialdehyde (MDA) + 4-hydroxyalkenals (4-HDA) and glutathione (GSH) levels were compared. Results: Pretreatment with SCH58261 significantly attenuated the decrease in Na+, K+-ATPase, decreased MDA+4-HDA levels and increased GSH in the HI-A2A group when compared to HIvehicle. Conclusion: A2A receptor activation may contribute to neuronal injury in newborn striatum after HI in association with decreased Na+, K+-ATPase activity and increased oxidative stress.

scholarly journals Characterization and partial purification of the sodium-potassium-ATPase inhibitor released from cultured rat hypothalamic cells.

1985 ◽  
Vol 260 (25) ◽  
pp. 13595-13600 ◽  
Author(s):  
K Morgan ◽  
M D Lewis ◽  
G Spurlock ◽  
P A Collins ◽  
S M Foord ◽  
...  
Keyword(s):  
Partial Purification ◽  
Atpase Inhibitor ◽  
Sodium Potassium ◽  
Hypothalamic Cells ◽  
Potassium Atpase
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