PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29237911-4	2017	SETTINGS AND DESIGN: This study was conducted to determine whether RET dysfunction involves an induced mutation into SK-N-MC cells.	sk-n-mc	117-124	ret proto-oncogene	Homo sapiens	67-70	
29237911-6	2017	SK-N-MC cells with different RET plasmids treated/untreated by GDNF, AKT and ERK1/2 phosphorylation detected by specific antibodies.	sk-n-mc	0-7	ret proto-oncogene	Homo sapiens	29-32	
29237911-8	2017	CONCLUSION: RET dysfunction involves an induced mutation into SK-N-MC cells.	sk-n-mc	62-69	ret proto-oncogene	Homo sapiens	12-15	
26065416-4	2015	Constitutive activation of RET in a SK-N-MC cell line model reduces cell sensitivity to chemotherapy.	sk-n-mc	36-43	ret proto-oncogene	Homo sapiens	27-30	
18751369-0	2008	RET activation inhibits doxorubicin-induced apoptosis in SK-N-MC cells.	sk-n-mc	57-64	ret proto-oncogene	Homo sapiens	0-3	
18751369-2	2008	MATERIALS AND METHODS: Each RET isoform was separately expressed in SK-N-MC cells (neural crest-derived tumor) and the impact of RET activation on doxorubicin-induced apoptosis was examined.	sk-n-mc	68-75	ret proto-oncogene	Homo sapiens	28-31	
18751369-3	2008	RESULTS: The activation of RET9 and RET51 in the SK-N-MC cells significantly reduced the doxorubicin-induced apoptosis by 50%, compared to untreated cells.	sk-n-mc	49-56	ret proto-oncogene	Homo sapiens	36-41	
18751369-6	2008	CONCLUSION: In SK-N-MC cells, downstream activation of MAP kinase, by both RET9 and RET51, appears to mediate the majority of RET-dependent resistance to chemotherapeutically induced apoptosis.	sk-n-mc	15-22	ret proto-oncogene	Homo sapiens	84-89	
18751369-6	2008	CONCLUSION: In SK-N-MC cells, downstream activation of MAP kinase, by both RET9 and RET51, appears to mediate the majority of RET-dependent resistance to chemotherapeutically induced apoptosis.	sk-n-mc	15-22	ret proto-oncogene	Homo sapiens	75-78	
7685595-4	1993	This result was confirmed by using a lysate of SK-N-MC human primitive neuroectodermal tumor cells transfected with the ret proto-oncogene.	sk-n-mc	47-54	ret proto-oncogene	Homo sapiens	120-123	
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	44-51	ret proto-oncogene	Homo sapiens	123-126	
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	44-51	ret proto-oncogene	Homo sapiens	142-145	
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	133-140	ret proto-oncogene	Homo sapiens	123-126	
12056817-2	2002	We found a high level of IL-8 production in SK-N-MC human primitive neuroectodermal tumor cells transfected with the human RET gene (SK-N-MC (RET) cells) in response to glial cell line-derived neurotrophic factor (GDNF) stimulation.	sk-n-mc	133-140	ret proto-oncogene	Homo sapiens	142-145	
12056817-4	2002	To investigate which signaling pathways are responsible for IL-8 expression, we treated SK-N-MC (RET) cells with several kinase inhibitors before GDNF stimulation.	sk-n-mc	88-95	ret proto-oncogene	Homo sapiens	97-100	
11535584-5	2001	Using the neuroectodermic SK-N-MC cell line, we found that the Ret tyrosine kinase activity is essential for GDNF to induce phosphatidylinositol 3-kinase (PI3K)/Akt and ERK pathways as well as cell rescue.	sk-n-mc	26-33	ret proto-oncogene	Homo sapiens	63-66	
9121763-0	1997	Cell scattering of SK-N-MC neuroepithelioma cells in response to Ret and FGF receptor tyrosine kinase activation is correlated with sustained ERK2 activation.	sk-n-mc	19-26	ret proto-oncogene	Homo sapiens	65-68