PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31030716-11	2019	P16 and P21 proteins had high expression in AngII, H2O2 and PA groups, most obviously in H2O2 group.	Hydrogen Peroxide	51-55	KRAS proto-oncogene, GTPase	Rattus norvegicus	8-11	
32582979-7	2020	In vitro, selective antagonism of MR partially blocked H2O2-induced myocardial aging as assessed by p16, p21 and p53 expression levels and excessive reactive oxygen species (ROS) accumulation.	Hydrogen Peroxide	55-59	KRAS proto-oncogene, GTPase	Rattus norvegicus	105-108	
31171766-7	2019	In vitro, H2O2 caused abnormal accumulation of progerin in nuclear and activation of nuclear p53-progerin interaction to trigger primary rat hepatocyte premature senescence through the p21-independent pathway; while these effects were rescued by prolonged exogenous IGF-1 or the IGF-1 adenovirus vector.	Hydrogen Peroxide	10-14	KRAS proto-oncogene, GTPase	Rattus norvegicus	185-188	
30802826-12	2019	Furthermore, luteolin alleviated H2O2-induced inactivation of PI3K/AKT pathway and activation of PDCD4/p21 pathway in PC-12 cells by up-regulating miR-21.	Hydrogen Peroxide	33-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	103-106	
30802826-15	2019	Luteolin protected PC-12 cells from H2O2-induced oxidative injury by up-regulating miR-21, activating PI3K/AKT pathway and inactivating PDCD4/p21 pathway.	Hydrogen Peroxide	36-40	KRAS proto-oncogene, GTPase	Rattus norvegicus	142-145	
33066270-7	2020	Artificial senescence induced by H2O2 caused a dose-dependent increase in Ccn3 gene and CCN3 protein expression, along with enhanced expression of p21 and p53 mRNA and proteins, as well as SA-beta gal activity.	Hydrogen Peroxide	33-37	KRAS proto-oncogene, GTPase	Rattus norvegicus	147-150	
31030716-11	2019	P16 and P21 proteins had high expression in AngII, H2O2 and PA groups, most obviously in H2O2 group.	Hydrogen Peroxide	89-93	KRAS proto-oncogene, GTPase	Rattus norvegicus	8-11	
21300357-5	2011	Pull-down assay or Western blot analysis revealed that pre-administration of 10(-8)mol/L E(2) significantly reduced the H(2)O(2)-induced activation of oncogene Ras, as well as activity of p16 and p38 MAPK, and expression of PRAK, p53, p21 and p-Rb.	Hydrogen Peroxide	120-128	KRAS proto-oncogene, GTPase	Rattus norvegicus	235-238	
29695641-5	2018	H2O2 mediated oxidative stress in 2G11 cells, a rat MPC clone previously established in our laboratory, successfully induced senescence, as shown by the upregulation of p21 and SASP factors, including IL-6.	Hydrogen Peroxide	0-4	KRAS proto-oncogene, GTPase	Rattus norvegicus	169-172	
24204728-7	2013	Interestingly, 1 nmol/L of BK almost completely inhibited the increase in senescent cell number and p21 expression induced by H2O2.	Hydrogen Peroxide	126-130	KRAS proto-oncogene, GTPase	Rattus norvegicus	100-103	
20495008-11	2010	Local activation of ERK1/2 by Ki-Ras stimulates mitochondrial SOD, which reduces reactive oxygen species and produces H(2)O(2).	Hydrogen Peroxide	118-126	KRAS proto-oncogene, GTPase	Rattus norvegicus	30-36	
33237045-7	2020	These effects were accompanied by attenuation of the H2O2-induced strengthening of the G2/M-phase inhibitory system, including increased mRNA and protein levels of cyclin-dependent kinase 1 (CDK1) and decreased p21 mRNA levels.	Hydrogen Peroxide	53-57	KRAS proto-oncogene, GTPase	Rattus norvegicus	211-214	
16901471-7	2006	p53 activation by H2O2 was evidenced by elevated Ser15 phosphorylation, increased luciferase p53 reporter activity and upregulation of the downstream p53 targets p21(waf1) and apoptotic proteins, bax, Noxa and PUMA.	Hydrogen Peroxide	18-22	KRAS proto-oncogene, GTPase	Rattus norvegicus	162-165