PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11884408-7	2002	We found that ROS production by V12-H-Ras expression was mediated by the Ras/phosphatidylinositol 3-kinase (PI3K)/Rac1/NADPH oxidase-dependent pathway and that pretreatment of V12-H-Ras-transformed cells with an antioxidant (N-acetylcysteine) and an NADPH oxidase inhibitor (diphenyleneiodonium) decreased DNA repair capacity.	Reactive Oxygen Species	14-17	Harvey rat sarcoma virus oncogene	Mus musculus	36-41	
12618760-4	2003	Our results demonstrate that overexpression of the inducible Ha-ras oncogene by isopropyl-beta-D-thiogalactoside (IPTG) increases the levels of reactive oxygen species (ROS, including O(2*-) and hydrogen peroxide (H(2)O(2))) and GSH in an Ha-ras-transformed NIH/3T3 fibroblast cell line.	Reactive Oxygen Species	144-167	Harvey rat sarcoma virus oncogene	Mus musculus	61-67	
12618760-4	2003	Our results demonstrate that overexpression of the inducible Ha-ras oncogene by isopropyl-beta-D-thiogalactoside (IPTG) increases the levels of reactive oxygen species (ROS, including O(2*-) and hydrogen peroxide (H(2)O(2))) and GSH in an Ha-ras-transformed NIH/3T3 fibroblast cell line.	Reactive Oxygen Species	169-172	Harvey rat sarcoma virus oncogene	Mus musculus	61-67	
12618760-4	2003	Our results demonstrate that overexpression of the inducible Ha-ras oncogene by isopropyl-beta-D-thiogalactoside (IPTG) increases the levels of reactive oxygen species (ROS, including O(2*-) and hydrogen peroxide (H(2)O(2))) and GSH in an Ha-ras-transformed NIH/3T3 fibroblast cell line.	Reactive Oxygen Species	169-172	Harvey rat sarcoma virus oncogene	Mus musculus	239-245	
24694812-5	2014	This potent cardioprotective effect resulted from strong suppression of H-Ras signaling activated by electrophilic stimulation with 8-nitro-cGMP functioning as a second messenger for the redox signaling induced by NO and ROS.	Reactive Oxygen Species	221-224	Harvey rat sarcoma virus oncogene	Mus musculus	72-77	
18005061-1	2007	In previous studies we found that the GTPase p21 Harvey-Ras (Ha-Ras) stimulates the production of reactive oxygen species and induces apoptosis by oxidative stress; this effect was reversed by farnesyl transferase inhibitors (FTIs).	Reactive Oxygen Species	98-121	Harvey rat sarcoma virus oncogene	Mus musculus	61-67	
11884408-7	2002	We found that ROS production by V12-H-Ras expression was mediated by the Ras/phosphatidylinositol 3-kinase (PI3K)/Rac1/NADPH oxidase-dependent pathway and that pretreatment of V12-H-Ras-transformed cells with an antioxidant (N-acetylcysteine) and an NADPH oxidase inhibitor (diphenyleneiodonium) decreased DNA repair capacity.	Reactive Oxygen Species	14-17	Harvey rat sarcoma virus oncogene	Mus musculus	180-185	
11884408-10	2002	Taken together, these results provide evidence that oncogenic H-Ras activates DNA repair capacity through the Ras/PI3K/Rac1/NADPH oxidase-dependent pathway and that increased ROS production via this signaling pathway is required for enhancement of the DNA repair capacity induced by oncogenic H-Ras.	Reactive Oxygen Species	175-178	Harvey rat sarcoma virus oncogene	Mus musculus	62-67	
11884408-10	2002	Taken together, these results provide evidence that oncogenic H-Ras activates DNA repair capacity through the Ras/PI3K/Rac1/NADPH oxidase-dependent pathway and that increased ROS production via this signaling pathway is required for enhancement of the DNA repair capacity induced by oncogenic H-Ras.	Reactive Oxygen Species	175-178	Harvey rat sarcoma virus oncogene	Mus musculus	293-298	
8954966-7	1996	In fact, inhibition of p21(ras) by transfecting E32-4-2 cells with the transdominant negative mutant of H-ras (L61, S186) led, analogously to lovastatin or (alpha-hydroxyfarnesyl) phosphonic acid treatment, to a strong increase of stress-induced ROS levels.	Reactive Oxygen Species	246-249	Harvey rat sarcoma virus oncogene	Mus musculus	104-109	
34204734-6	2021	Conversely, knockdown of CUX1, CUX2, or SATB1 was found to be synthetic lethal in cancer cells exhibiting high ROS levels as a consequence of activating mutations in KRAS, HRAS, BRAF, or EGFR.	Reactive Oxygen Species	111-114	Harvey rat sarcoma virus oncogene	Mus musculus	172-176