PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33562061-7	2021	An increase in oxidative stress, characterized by decreased nuclear factor E2-related factor 2 (NRF2) protein levels and aconitase activity and increased H2O2 levels were also found in the brain of IGF1R-deficient mice.	Hydrogen Peroxide	154-158	insulin-like growth factor I receptor	Mus musculus	198-203	
25406880-7	2014	CONCLUSION: Down-regulating miR-100 is an effective method to protect H2O2 induced apoptosis in RGC-5 cells, possible associated with IGF1R regulation.	Hydrogen Peroxide	70-74	insulin-like growth factor I receptor	Mus musculus	134-139	
25783760-7	2015	Silencing IGF-1R enhanced the influence of H2O2 in disrupting the VE-protein tyrosine phosphatase/VE-cadherin interaction.	Hydrogen Peroxide	43-47	insulin-like growth factor I receptor	Mus musculus	10-16	
25783760-8	2015	Overexpression of IGF-1R suppressed H2O2-induced endothelial barrier dysfunction.	Hydrogen Peroxide	36-40	insulin-like growth factor I receptor	Mus musculus	18-24	
26191255-7	2015	More importantly, ectopic down-regulation of IGF1R reversed the protective effect of miR-100 down-regulation on H2O2-induced apoptosis, revealing that miR-100 regulates cardiomyocyte apoptosis through the association of IGF1R.	Hydrogen Peroxide	112-116	insulin-like growth factor I receptor	Mus musculus	45-50	
26191255-7	2015	More importantly, ectopic down-regulation of IGF1R reversed the protective effect of miR-100 down-regulation on H2O2-induced apoptosis, revealing that miR-100 regulates cardiomyocyte apoptosis through the association of IGF1R.	Hydrogen Peroxide	112-116	insulin-like growth factor I receptor	Mus musculus	220-225	
23675509-4	2013	Treating the IGF-1R deficient myoblasts with H2O2 resulted in significantly higher phosphorylation of Akt as compared to cells having normal expression of IGF-1R.	Hydrogen Peroxide	45-49	insulin-like growth factor I receptor	Mus musculus	13-19	
23675509-4	2013	Treating the IGF-1R deficient myoblasts with H2O2 resulted in significantly higher phosphorylation of Akt as compared to cells having normal expression of IGF-1R.	Hydrogen Peroxide	45-49	insulin-like growth factor I receptor	Mus musculus	155-161	
23675509-8	2013	However, in NIH-3T3 fibroblasts and MC3T3-E1 osteoblasts, the loss of IGF-1R by siRNA directed knockdown was associated with reduced levels of phosphorylated Akt on treatment with H2O2 or UV as compared to control cells and these cells showed more apoptosis.	Hydrogen Peroxide	180-184	insulin-like growth factor I receptor	Mus musculus	70-76