PPP1R1A Human

I-1 was the first endogenous molecule identified to specifically inhibit PP-1 . It is activated by cAMP-dependent protein kinase A (PKA), which prevents the dephosphorylation of target proteins by PP-1, thereby amplifying β-adrenoceptor (β-AR) signaling . This signaling pathway is vital for heart function, and dysregulation can lead to heart failure and arrhythmias .

In physiological conditions, I-1 helps maintain proper cardiac function by regulating the phosphorylation state of various proteins involved in heart muscle contraction and relaxation . However, in pathological conditions such as heart failure and atrial fibrillation, I-1 is often down-regulated and hypo-phosphorylated, leading to impaired cardiac function . Conversely, in some cases of atrial fibrillation, I-1 can become hyperactive, contributing to the disease’s progression .

Given its critical role in cardiac function, I-1 has been suggested as a potential therapeutic target for heart diseases . Research involving genetic mouse models has provided insights into the therapeutic potential of modulating I-1 activity to treat heart failure and arrhythmias .

Recombinant I-1 is produced using recombinant DNA technology, which involves inserting the gene encoding I-1 into a host organism, such as bacteria or yeast, to produce the protein in large quantities . This recombinant form is used in various research and therapeutic applications, including studies on cardiac function and potential treatments for heart diseases .