PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26374610-5	2016	In Pkd2(-/WS25) mice, knockout of Pde1a, Pde1c, or Pde3a but not of Pde1b or Pde3b aggravated the development of PKD and was associated with higher levels of protein kinase A-phosphorylated (Ser133) cAMP-responsive binding protein (P-CREB), activating transcription factor-1, and CREB-induced CRE modulator proteins in kidney nuclear preparations.	Cyclic AMP	199-203	phosphodiesterase 1A, calmodulin-dependent	Mus musculus	34-39	
26374610-5	2016	In Pkd2(-/WS25) mice, knockout of Pde1a, Pde1c, or Pde3a but not of Pde1b or Pde3b aggravated the development of PKD and was associated with higher levels of protein kinase A-phosphorylated (Ser133) cAMP-responsive binding protein (P-CREB), activating transcription factor-1, and CREB-induced CRE modulator proteins in kidney nuclear preparations.	Cyclic AMP	199-203	phosphodiesterase 3A, cGMP inhibited	Mus musculus	51-56	
26374610-8	2016	These observations show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the development of PKD, possibly through the regulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secretion.	Calcium	29-36	phosphodiesterase 1A, calmodulin-dependent	Mus musculus	69-74	
26374610-8	2016	These observations show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the development of PKD, possibly through the regulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secretion.	Calcium	29-36	phosphodiesterase 1C	Mus musculus	79-84	
26374610-8	2016	These observations show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the development of PKD, possibly through the regulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secretion.	Calcium	29-36	cystic fibrosis transmembrane conductance regulator	Mus musculus	229-233	
26374610-8	2016	These observations show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the development of PKD, possibly through the regulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secretion.	Cyclic AMP	182-186	phosphodiesterase 1A, calmodulin-dependent	Mus musculus	69-74	
26374610-8	2016	These observations show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the development of PKD, possibly through the regulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secretion.	Cyclic AMP	182-186	phosphodiesterase 1C	Mus musculus	79-84	
26374610-8	2016	These observations show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the development of PKD, possibly through the regulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secretion.	Cyclic AMP	182-186	phosphodiesterase 3A, cGMP inhibited	Mus musculus	90-95	
26374610-8	2016	These observations show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the development of PKD, possibly through the regulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secretion.	Cyclic AMP	182-186	cystic fibrosis transmembrane conductance regulator	Mus musculus	229-233