PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18285460-3	2008	The depletion of Rvb1 increases the amount and persistence of phosphorylation on chromatin-associated H2AX after the exposure of cells to UV irradiation or to mitomycin C, cisplatin, camptothecin, or etoposide, without increasing the amount of DNA damage.	Mitomycin	159-170	H2A.X variant histone	Homo sapiens	102-106	
23580445-6	2013	In particular, the compound labeled NSC 130813 [4-[(6-chloro-2-methoxy-9-acridinyl)amino]-2-[(4-methyl-1-piperazinyl)methyl]] was shown to act synergistically with cisplatin and mitomycin C; to increase UVC-mediated cytotoxicity; to modify DNA repair as indicated by the staining of phosphorylated H2AX; and to disrupt interaction between ERCC1 and XPF in cells.	Mitomycin	178-189	H2A.X variant histone	Homo sapiens	298-302	
27174706-3	2016	Thus, we investigated DSBs repair efficiency in a group of obese adolescents assessing the kinetic of H2AX phosphorylation in mitomycin C (MMC)-treated lymphocytes harvested 2 h- or 4 h-post mutagen treatment.	Mitomycin	126-137	H2A.X variant histone	Homo sapiens	102-106	
27174706-3	2016	Thus, we investigated DSBs repair efficiency in a group of obese adolescents assessing the kinetic of H2AX phosphorylation in mitomycin C (MMC)-treated lymphocytes harvested 2 h- or 4 h-post mutagen treatment.	Mitomycin	139-142	H2A.X variant histone	Homo sapiens	102-106	
27076919-9	2016	Consistent with these cytotoxic profiles, cisplatin/mitomycin C, triapine, and paclitaxel differed in the capacity to induce phosphorylation of H2AX, and produced unique inhibitory patterns of DNA/RNA syntheses in HL-60 human leukemia cells.	Mitomycin	52-63	H2A.X variant histone	Homo sapiens	144-148	
23696313-0	2013	Kinetics of nuclear phosphorylation (gamma-H2AX) in human lymphocytes treated in vitro with UVB, bleomycin and mitomycin C.	Mitomycin	111-122	H2A.X variant histone	Homo sapiens	43-47	
23696313-4	2013	Here, we investigated the time-course of gamma-H2AX in unstimulated or cultured peripheral lymphocytes in vitro treated with UVB, bleomycin and mitomycin C (MMC).	Mitomycin	144-155	H2A.X variant histone	Homo sapiens	47-51	
23696313-4	2013	Here, we investigated the time-course of gamma-H2AX in unstimulated or cultured peripheral lymphocytes in vitro treated with UVB, bleomycin and mitomycin C (MMC).	Mitomycin	157-160	H2A.X variant histone	Homo sapiens	47-51	
17167777-2	2007	The results showed that MMC treatment arrested the cells in S-phase and induced the appearance of gamma-H2AX and Rad51 nuclear foci, accompanied with a sequestering of Rad51 to the nuclear matrix.	Mitomycin	24-27	H2A.X variant histone	Homo sapiens	104-108	
15199134-7	2004	Treatment of wild-type cells with mitomycin C (MMC) induced gamma-H2AX foci and increased the amount of DSBs detected by pulsed-field gel electrophoresis.	Mitomycin	34-45	H2A.X variant histone	Homo sapiens	60-70	
15199134-7	2004	Treatment of wild-type cells with mitomycin C (MMC) induced gamma-H2AX foci and increased the amount of DSBs detected by pulsed-field gel electrophoresis.	Mitomycin	47-50	H2A.X variant histone	Homo sapiens	60-70	
15199134-8	2004	Surprisingly, gamma-H2AX foci were also induced in Ercc1(-/-) cells by MMC treatment.	Mitomycin	71-74	H2A.X variant histone	Homo sapiens	14-24	
15199134-11	2004	In Ercc1(-/-) cells, MMC-induced gamma-H2AX foci persisted at least 48 h longer than in wild-type cells, demonstrating that Ercc1 is required for the resolution of cross-link-induced DSBs.	Mitomycin	21-24	H2A.X variant histone	Homo sapiens	33-43