PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18007024-8	2008	Taken together, our findings identify a novel mechanism by which myocardial nNOS promotes left ventricular relaxation by regulating the protein kinase A-mediated phosphorylation of PLN and the rate of sarcoplasmic reticulum Ca2+ reuptake via a cGMP-independent effect on protein phosphatase activity.	Cyclic GMP	244-248	phospholamban	Mus musculus	181-184	
21945464-5	2012	Conversely, nNOS-derived NO regulates basal myocardial inotropy and relaxation by inhibiting the sarcolemmal Ca(2+) current (I(Ca)) and promoting protein kinase A-dependent phospholamban (PLN) phosphorylation, independent of cGMP.	Cyclic GMP	225-229	phospholamban	Mus musculus	188-191	
22484619-9	2012	Conversely, inhibition of cGMP/PKG pathway abolished the Ang II-induced faster relaxation by reducing phospholamban (PLN) Ser(16) phosphorylation.	Cyclic GMP	26-30	phospholamban	Mus musculus	117-120