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dATP can increase contractility as well as systolic pressure in a failing heart and that it can also enhance contraction as well as restoring the cardiac pump function. Further, dATP has been found not only to restore normal systolic function in patients with cardiovascular impairments but that it can also increase contraction, as well as the rate of cross-bridge of the cardiac muscle of patients in their end-stage congestive heart failure without hindering, or impairing the systolic relaxation.

dATP inhibition of Ribonucleotide reductases

The class Ia Ribonucleotide reductase of the E.coli confirms that dATP regulates the activities of the Ribonucleotide reductase by binding to the A site of the nucleotide binding sites. The inhibition of the class Ia Ribonucleotide reductase of the E. coli by the dATP is due to the increased space between the cysteine and tyrosine radical cofactor in C-site and 𝛃2 respectively, which in turn inhibits the formation of the active site which is usually necessary reduction. In human Ribonucleotide reductase, dATP induced α6 structure inhibits the activity of the Ribonucleotide reductase by preventing 𝛃 subunit from accessing the active site of the of 𝛂 subunit.