PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19587996-1	2009	NMR spectroscopy was used to study the interaction of Ni(II) ions with C-terminal sequence of Cap43 protein where, from Thr341 to Gly360 residue, a T1R2S3R4S5H6T7S8E9G10 ten-amino acid fragment is consecutively repeated three times.	Nickel(2+)	54-60	N-myc downstream regulated 1	Homo sapiens	94-99	
10910041-3	2000	We found that the exposure of A549 cells to Co2+ or Ni2+ produced oxidative stress, and although Co2+ was a more potent producer of ROS than Ni2+, both metals equally increased the expression of Cap43, a hypoxia-regulated gene.	Nickel(2+)	52-56	N-myc downstream regulated 1	Homo sapiens	195-200	
15149799-0	2004	Nickel(II) binding to Cap43 protein fragments.	Nickel(2+)	0-10	N-myc downstream regulated 1	Homo sapiens	22-27	
11330481-0	2001	Ni(II) and Cu(II) binding with a 14-aminoacid sequence of Cap43 protein, TRSRSHTSEGTRSR.	Nickel(2+)	0-6	N-myc downstream regulated 1	Homo sapiens	58-63	
11330481-1	2001	The tetradecapeptide containing the 10 aminoacid repeated sequence on the C-terminus of the Ni(II)-induced Cap43 protein, was analyzed for Ni(II) and Cu(II) binding.	Nickel(2+)	92-98	N-myc downstream regulated 1	Homo sapiens	107-112	
10910041-3	2000	We found that the exposure of A549 cells to Co2+ or Ni2+ produced oxidative stress, and although Co2+ was a more potent producer of ROS than Ni2+, both metals equally increased the expression of Cap43, a hypoxia-regulated gene.	Nickel(2+)	141-145	N-myc downstream regulated 1	Homo sapiens	195-200	
9605764-0	1998	Cap43, a novel gene specifically induced by Ni2+ compounds.	Nickel(2+)	44-48	N-myc downstream regulated 1	Homo sapiens	0-5	
9605764-9	1998	We have found that the primary signal for Cap43 induction was an elevation of free intracellular Ca2+ caused by Ni2+ exposure because Cap43 was induced by calcium ionophores and its induction was attenuated by bis-(O-aminophenyl)-ethane-N,N,N",N"-tetraacetic acid tetra(acetoxymethyl)-ester, a chelator of intracellular Ca2+.	Nickel(2+)	112-116	N-myc downstream regulated 1	Homo sapiens	42-47	
9605764-9	1998	We have found that the primary signal for Cap43 induction was an elevation of free intracellular Ca2+ caused by Ni2+ exposure because Cap43 was induced by calcium ionophores and its induction was attenuated by bis-(O-aminophenyl)-ethane-N,N,N",N"-tetraacetic acid tetra(acetoxymethyl)-ester, a chelator of intracellular Ca2+.	Nickel(2+)	112-116	N-myc downstream regulated 1	Homo sapiens	134-139