PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8927709-3	1996	The cell line IGR39D was transfected with the MYC oncogene, the proto-oncogene NRAS, NRAS activated by a point mutation (61-arginine) or a combination of mutated NRAS and MYC.	Arginine	124-132	NRAS proto-oncogene, GTPase	Homo sapiens	85-89	
2247846-6	1990	These mutations would result in amino acid substitutions of lysine, leucine, or arginine for the normal glutamine at position 61 in the N-ras protein.	Arginine	80-88	NRAS proto-oncogene, GTPase	Homo sapiens	136-141	
3038106-2	1987	Analysis using synthetic 20-mer oligonucleotide probes revealed a point mutation from G to C at the first letter of codon 13 of the N-ras gene resulting in the substitution of arginine for glycine.	Arginine	176-184	NRAS proto-oncogene, GTPase	Homo sapiens	132-137	
3102434-3	1987	Nucleotide sequence analysis of the activated N-ras showed a single G----C point mutation at the first letter of codon 13, resulting in the coding of arginine instead of glycine.	Arginine	150-158	NRAS proto-oncogene, GTPase	Homo sapiens	46-51	
15688405-4	2005	Using both small interfering RNA- and plasmid based-RNA interference techniques, oncogenic NRAS was specifically suppressed in 2 human melanoma cell lines, 224 and BL, which harbor a codon 61 CAA (glutamine) to CGA (arginine) NRAS mutation.	Arginine	216-224	NRAS proto-oncogene, GTPase	Homo sapiens	91-95	
12783933-9	2003	RESULTS: Activating mutations in NRAS codon 61, all of which were either CAA(Gln)-AAA(Lys) or CAA(Gln)-CGA(Arg) mutations, were found in 95% (20/21) of primary hereditary melanomas but in only 10% (1/10) of sporadic melanomas (P<.001).	Arginine	107-110	NRAS proto-oncogene, GTPase	Homo sapiens	33-37	
10465111-4	1999	Activating point mutations in the N-ras gene (nine CAA (Gln) to AAA (Lys) transversions and one CAA (Gln) to CGA (Arg) transition at codon 61) were detected at high frequency (56%).	Arginine	114-117	NRAS proto-oncogene, GTPase	Homo sapiens	34-39	
8927709-3	1996	The cell line IGR39D was transfected with the MYC oncogene, the proto-oncogene NRAS, NRAS activated by a point mutation (61-arginine) or a combination of mutated NRAS and MYC.	Arginine	124-132	NRAS proto-oncogene, GTPase	Homo sapiens	85-89	
7627974-3	1995	To study the role of N-ras-activating mutations in the regulation of myeloma tumor growth, we introduced a constitutively active N-ras cDNA containing a glutamine to arginine (CAA-CGA) amino acid substitution at codon 61 into the interleukin 6 (IL-6)-dependent myeloma cell line ANBL6.	Arginine	166-174	NRAS proto-oncogene, GTPase	Homo sapiens	129-134	
8062279-2	1994	Five of these clones and the parental cell line showed a mutation at codon 61 of N-RAS that resulted in Gln-->Arg substitution (N-RAS/61+), while in the remaining 14, only the wild-type allele for N-RAS was present (N-RAS/61-).	Arginine	113-116	NRAS proto-oncogene, GTPase	Homo sapiens	81-86	
7725728-8	1994	All mutations detected were adenine to guanine transitions at the second position of N-ras codon 61, resulting in a conversion from glutamine to arginine.	Arginine	145-153	NRAS proto-oncogene, GTPase	Homo sapiens	85-90	
8032213-3	1994	A panel of 21 clones deriving from the metastatic lesion Me665/2, which had a Gln-->Arg substitution at codon 61 of N-RAS (N-RAS/61+), were also examined.	Arginine	87-90	NRAS proto-oncogene, GTPase	Homo sapiens	119-124