Disease relevance of ATPIF1

• Brief episodes of ischemia in dogs induce stunning as well as IP [1].
• One or several brief episodes of myocardial ischemia (ischemic preconditioning; IP) rapidly induces tolerance to a later ischemic challenge [1].
• Hypertensive diabetic patients with a positive family history for hypertension had high ATPI levels compared with those patients with a negative family history for the disease [2].

High impact information on ATPIF1

• Therefore, it is probable that the function of IP in the plasma membrane of endothelial cells is not limited to regulation of catalysis [3].
• TNF-alpha decreases the level of beta-subunits and increases the amount of IP, indicating that the ratio of IP to beta-subunit exhibits significant variations [3].
• The most active species, 1, 5, 6,10,11 and 12 exhibited strongly negative charged atoms over the C6 and C7 positions, the higher IP, higher mu and higher energy gap [4].
• High homology of two internal peptides of IP with known plant sucrose synthase (SS) sequences suggested that IP might be related somehow with SS [5].
• Several mechanisms for IP and the associated metabolic slowing have been studied: The mitochondrial ATPase is a major cause of ATP hydrolysis in ischemic myocardium but slower ATP depletion in preconditioned myocardium is not due to persistent inhibition of this ATPase [1].

Biological context of ATPIF1

• From these results it is suggested that circulating Na-K-ATPase inhibitor (plasma ATPI) may be involved in the regulation of the circadian rhythm of urinary Na excretion [6].
• In order to study the biological activity of endogenous digitalis-like substance (DLS) and Na-K-ATPase inhibitor (ATPI), human urine was partially purified and administered to rats, and its effects on the urinary volume, urinary Na excretion and blood pressure (BP) were determined [7].
• Hyperbaric oxygen mediates the effects of ATPI through four mechanisms: hyperoxygenation, vasoconstriction, reperfusion, and host factors [8].

Anatomical context of ATPIF1

• Plasma membranes have the capacity to bind exogenous IP [3].
• The ATPase inhibitor protein (IP) of mitochondria was detected in the plasma membrane of living endothelial cells by flow cytometry, competition assays, and confocal microscopy of cells exposed to IP antibodies [3].
• Shortening of the IP duration was correlated to degree of upper limb spasticity (Ashworth scale) and may be due to supraspinal level reduction of the inhibitory function [9].

Associations of ATPIF1 with chemical compounds

• Follow-up measurement was not performed according to the ATPI schedule, and the magnitude of cholesterol response was inversely related to time to first follow-up measurement [10].
• The chloroform layer was applied to an open silica gel column, and at a fraction with ethylacetate: methanol (60: 40, T-1 fraction), DLS and ATPI were eluted at the highest concentration [7].

Analytical, diagnostic and therapeutic context of ATPIF1

• IP was purified by gel filtration on Superose 12 and preparative SDS-PAGE, and specific antibodies were prepared [11].
• After gel filtration on Superose 12, IP yielded a major polypeptide of about 80 kDa on SDS-PAGE [11].
• A cross-sectional analysis was conducted to test the feasibility of the National Cholesterol Education Program Adult Treatment Panel I Guidelines (ATPI) in physician office practices [10].
• IP and SS activities were found in the same preparation and showed thermolability between 60-65 degrees C. IP and SS activities presented the same ionic charge and molecular mass in native conditions (Mono Q and Superose-12 columns chromatographies) [5].
• Western blot experiments with an anti-SS antibody as well as with an anti-IP antibody showed a single 80 kDa polypeptide band where IP and SS activities were present [5].

References