PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18006504-0	2008	A MAPK-positive feedback mechanism for BLR1 signaling propels retinoic acid-triggered differentiation and cell cycle arrest.	Tretinoin	62-75	mitogen-activated protein kinase 1	Homo sapiens	2-6	
18006504-1	2008	MAPK signaling is required for retinoic acid (RA)-triggered G(0) cell cycle arrest and cell differentiation, but the mechanism is not well defined.	Tretinoin	31-44	mitogen-activated protein kinase 1	Homo sapiens	0-4	
18006504-1	2008	MAPK signaling is required for retinoic acid (RA)-triggered G(0) cell cycle arrest and cell differentiation, but the mechanism is not well defined.	Tretinoin	46-48	mitogen-activated protein kinase 1	Homo sapiens	0-4	
18006504-2	2008	In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition.	Tretinoin	15-17	mitogen-activated protein kinase 1	Homo sapiens	36-40	
18006504-2	2008	In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition.	Tretinoin	15-17	mitogen-activated protein kinase 1	Homo sapiens	96-99	
18006504-2	2008	In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition.	Tretinoin	15-17	mitogen-activated protein kinase 1	Homo sapiens	114-118	
18006504-4	2008	Unlike wild-type parental cells, RA-treated BLR1 knock-out cells failed to show RAF and consequential MEK and ERK phosphorylation, failed to accumulate CDK inhibitors that control G(1)/S transition, and failed to differentiate and arrest in response to RA, whereas ectopically overexpressing BLR1 enhanced MAPK signaling and caused accelerated RA-induced differentiation and arrest.	Tretinoin	33-35	mitogen-activated protein kinase 1	Homo sapiens	306-310	
18006504-6	2008	Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest.	Tretinoin	26-28	mitogen-activated protein kinase 1	Homo sapiens	110-114	
18006504-6	2008	Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest.	Tretinoin	26-28	mitogen-activated protein kinase 1	Homo sapiens	199-203	
18006504-7	2008	Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation.	Tretinoin	16-18	mitogen-activated protein kinase 1	Homo sapiens	96-100	
18006504-7	2008	Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation.	Tretinoin	16-18	mitogen-activated protein kinase 1	Homo sapiens	213-217	
18006504-7	2008	Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation.	Tretinoin	239-241	mitogen-activated protein kinase 1	Homo sapiens	96-100	
18006504-7	2008	Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation.	Tretinoin	239-241	mitogen-activated protein kinase 1	Homo sapiens	213-217