PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
23755964-5	2013	GD NEIL3 excised the hydantoin lesions spiroiminodihydantoin (Sp) and guanidinohydantoin (Gh) in single-stranded (ss) and double-stranded (ds) DNA efficiently.	sp	39-60	nei like DNA glycosylase 3	Homo sapiens	3-8
32302101-7	2020	The primary factor that recognizes DNA lesions is the DNA damage-sensing factor XPC-RAD23B (XPC), while the glycosylase NEIL1 is known to remove Gh and Sp lesions from double-stranded DNA.	sp	152-154	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	80-90
32302101-7	2020	The primary factor that recognizes DNA lesions is the DNA damage-sensing factor XPC-RAD23B (XPC), while the glycosylase NEIL1 is known to remove Gh and Sp lesions from double-stranded DNA.	sp	152-154	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	80-83
32302101-7	2020	The primary factor that recognizes DNA lesions is the DNA damage-sensing factor XPC-RAD23B (XPC), while the glycosylase NEIL1 is known to remove Gh and Sp lesions from double-stranded DNA.	sp	152-154	nei like DNA glycosylase 1	Homo sapiens	120-125
32302101-11	2020	However, upon progressively increasing the XPC concentration, the amplitude of the burst phase decreases gradually, and a slower time-dependent phase of incision product formation manifests itself with rate constants of 3.0x10-3 (Gh) and 0.90x10-3 s-1 (Sp).	sp	253-255	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	43-46
32302101-12	2020	These slow kinetics are attributed to the dissociation of XPC-DNA complexes that allow for the rebinding of NEIL1 to the temporarily exposed Gh or Sp lesions, and the incisions observed under these steady-state conditions.	sp	147-149	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	58-61
32302101-12	2020	These slow kinetics are attributed to the dissociation of XPC-DNA complexes that allow for the rebinding of NEIL1 to the temporarily exposed Gh or Sp lesions, and the incisions observed under these steady-state conditions.	sp	147-149	nei like DNA glycosylase 1	Homo sapiens	108-113
27880870-8	2017	This review focuses on initiation of BER by the mammalian Nei-like1-3 (NEIL1-3) glycosylases for removal of 2Ih, Sp, and Gh.	sp	113-115	nei like DNA glycosylase 2	Homo sapiens	58-69
27880870-8	2017	This review focuses on initiation of BER by the mammalian Nei-like1-3 (NEIL1-3) glycosylases for removal of 2Ih, Sp, and Gh.	sp	113-115	nei like DNA glycosylase 1	Homo sapiens	71-76
28230976-4	2017	Duplexes containing (S)-Sp consistently gave deeper current blockage, and a baseline resolution of ~0.8 pA was achieved between (S)-Sp:G and (R)-Sp:G base pairs.	sp	20-26	surfactant associated 2	Homo sapiens	132-136
28230976-4	2017	Duplexes containing (S)-Sp consistently gave deeper current blockage, and a baseline resolution of ~0.8 pA was achieved between (S)-Sp:G and (R)-Sp:G base pairs.	sp	20-26	surfactant associated 2	Homo sapiens	145-149
24649945-0	2014	Crystal structure of DNA polymerase beta with DNA containing the base lesion spiroiminodihydantoin in a templating position.	sp	77-98	DNA polymerase beta	Homo sapiens	21-40
24649945-1	2014	The first high-resolution crystal structure of spiroiminodihydantoin (dSp1) was obtained in the context of the DNA polymerase beta active site and reveals two areas of significance.	sp	47-68	Sp1	Drosophila melanogaster	70-74
24649945-1	2014	The first high-resolution crystal structure of spiroiminodihydantoin (dSp1) was obtained in the context of the DNA polymerase beta active site and reveals two areas of significance.	sp	47-68	DNA polymerase beta	Homo sapiens	111-130
23755964-5	2013	GD NEIL3 excised the hydantoin lesions spiroiminodihydantoin (Sp) and guanidinohydantoin (Gh) in single-stranded (ss) and double-stranded (ds) DNA efficiently.	sp	62-64	nei like DNA glycosylase 3	Homo sapiens	3-8
16022506-7	2005	Trapping of the guanine lesions by the base excision repair enzymes hOGG1 and mNEIL2 showed nearly exclusive trapping by mNEIL2, suggesting that 8-oxoG was not the major lesion but rather a lesion recognized by mNEIL2 such as Sp.	sp	226-228	8-oxoguanine DNA glycosylase	Homo sapiens	68-73
20099873-1	2010	Human DNA glycosylase NEIL1 exhibits a superior ability to remove oxidized guanine lesions guanidinohydantoin (Gh) and spiroiminodihydantoin (Sp) from duplex DNA in comparison to other substrates.	sp	119-140	nei like DNA glycosylase 1	Homo sapiens	22-27
20099873-1	2010	Human DNA glycosylase NEIL1 exhibits a superior ability to remove oxidized guanine lesions guanidinohydantoin (Gh) and spiroiminodihydantoin (Sp) from duplex DNA in comparison to other substrates.	sp	142-144	nei like DNA glycosylase 1	Homo sapiens	22-27
20099873-2	2010	In this work, Gh and Sp lesions in bubble, bulge, and single-stranded DNA were found to be good substrates for NEIL1 but were typically excised at much slower rates than from canonical duplex substrates.	sp	21-23	nei like DNA glycosylase 1	Homo sapiens	111-116
23926102-5	2013	Although Sp and Gh in quadruplex DNA were good substrates for mNeil3 and NEIL1, none of the glycosylases had activity on quadruplex DNA containing 8-oxoG.	sp	9-11	nei like 3 (E. coli)	Mus musculus	62-68
23926102-5	2013	Although Sp and Gh in quadruplex DNA were good substrates for mNeil3 and NEIL1, none of the glycosylases had activity on quadruplex DNA containing 8-oxoG.	sp	9-11	nei like DNA glycosylase 1	Homo sapiens	73-78
18543945-2	2008	Of these, the hydantoin lesions, guanidinohydantoin (Gh) and the two diastereomers of spiroiminodihydantoin (Sp1 and Sp2), have garnered much recent attention due to their unusual structures, high mutagenic potential, and detection in cells.	sp	86-107	Sp2 transcription factor	Homo sapiens	117-120
17432829-4	2007	To elucidate structural properties determining hNeil1"s substrate specificities, we have investigated it in complex with two pairs of representative well-repaired substrates: the R- and S-spiroiminodihydantoin (Sp) stereoisomers, nonplanar further oxidation products of guanine, and the 5R,6S- and 5S,6R-thymine glycol (Tg) stereoisomers, the most prevalent oxidative lesions of thymine.	sp	211-213	nei like DNA glycosylase 1	Homo sapiens	47-53
16022506-7	2005	Trapping of the guanine lesions by the base excision repair enzymes hOGG1 and mNEIL2 showed nearly exclusive trapping by mNEIL2, suggesting that 8-oxoG was not the major lesion but rather a lesion recognized by mNEIL2 such as Sp.	sp	226-228	nei like 2 (E. coli)	Mus musculus	78-84
16022506-7	2005	Trapping of the guanine lesions by the base excision repair enzymes hOGG1 and mNEIL2 showed nearly exclusive trapping by mNEIL2, suggesting that 8-oxoG was not the major lesion but rather a lesion recognized by mNEIL2 such as Sp.	sp	226-228	nei like 2 (E. coli)	Mus musculus	121-127
16022506-7	2005	Trapping of the guanine lesions by the base excision repair enzymes hOGG1 and mNEIL2 showed nearly exclusive trapping by mNEIL2, suggesting that 8-oxoG was not the major lesion but rather a lesion recognized by mNEIL2 such as Sp.	sp	226-228	nei like 2 (E. coli)	Mus musculus	121-127
16022506-8	2005	Formation of the Sp lesion in the Cr(VI)/Asc oxidation reaction with DNA was confirmed by LC-ESI-MS detection.	sp	17-19	steroid sulfatase	Homo sapiens	41-44
16022506-10	2005	Concentrations of Cr(VI) (3.1-50 microM) with a corresponding 1:10 ratio of Asc oxidized between 0.3% and 1.5% of all guanines within the duplex DNA strand to Sp.	sp	159-161	steroid sulfatase	Homo sapiens	76-79
15533836-0	2005	Recognition of the oxidized lesions spiroiminodihydantoin and guanidinohydantoin in DNA by the mammalian base excision repair glycosylases NEIL1 and NEIL2.	sp	36-57	nei like DNA glycosylase 1	Homo sapiens	139-144
15533836-0	2005	Recognition of the oxidized lesions spiroiminodihydantoin and guanidinohydantoin in DNA by the mammalian base excision repair glycosylases NEIL1 and NEIL2.	sp	36-57	nei like DNA glycosylase 2	Homo sapiens	149-154
15533836-7	2005	Herein we report that two recently identified mammalian glycosylases, NEIL1 and NEIL2, showed a high affinity for recognition and cleavage of DNA containing Gh/Ia and Sp lesions.	sp	167-169	nei like DNA glycosylase 1	Homo sapiens	70-75
15533836-7	2005	Herein we report that two recently identified mammalian glycosylases, NEIL1 and NEIL2, showed a high affinity for recognition and cleavage of DNA containing Gh/Ia and Sp lesions.	sp	167-169	nei like DNA glycosylase 2	Homo sapiens	80-85
15533836-10	2005	NEIL1 was able to excise the Sp lesion opposite the four natural bases in double-stranded DNA, however, NEIL2 showed little cleavage activity against the Sp lesion in duplex DNA although DNA trapping studies show recognition and binding of NEIL2 to this lesion.	sp	29-31	nei like DNA glycosylase 1	Homo sapiens	0-5
34060590-1	2021	The oxidatively generated genotoxic spiroiminodihydantoin (Sp) lesions are well-known substrates of base excision repair (BER) pathway initiated by the bifunctional DNA glycosylase NEIL1.	sp	36-57	nei like DNA glycosylase 1	Homo sapiens	181-186
14503888-6	2003	In contrast, both yOGG1 and yOGG2 enzymes removed Gh and Sp in a relatively efficient manner from an 18 bp duplex.	sp	57-59	8-oxoguanine glycosylase OGG1	Saccharomyces cerevisiae S288C	18-23
14503888-6	2003	In contrast, both yOGG1 and yOGG2 enzymes removed Gh and Sp in a relatively efficient manner from an 18 bp duplex.	sp	57-59	bifunctional N-glycosylase/AP lyase NTG1	Saccharomyces cerevisiae S288C	28-33
14503888-8	2003	However, yOGG2 removed Sp at a faster rate than Gh.	sp	23-25	bifunctional N-glycosylase/AP lyase NTG1	Saccharomyces cerevisiae S288C	9-14
34060590-1	2021	The oxidatively generated genotoxic spiroiminodihydantoin (Sp) lesions are well-known substrates of base excision repair (BER) pathway initiated by the bifunctional DNA glycosylase NEIL1.	sp	59-61	nei like DNA glycosylase 1	Homo sapiens	181-186
34060590-2	2021	In this work we reported that the excision kinetics of the single Sp lesions site-specifically embedded in the covalently closed circular DNA plasmids (contour length 2686 base pairs) by NEIL1 are biphasic under single-turnover conditions ((NEIL1)>>(SpDNApl)) in contrast to monophasic excision kinetics of the same lesions embedded in147-mer Sp-modified DNA duplexes.	sp	66-68	nei like DNA glycosylase 1	Homo sapiens	187-192
34060590-2	2021	In this work we reported that the excision kinetics of the single Sp lesions site-specifically embedded in the covalently closed circular DNA plasmids (contour length 2686 base pairs) by NEIL1 are biphasic under single-turnover conditions ((NEIL1)>>(SpDNApl)) in contrast to monophasic excision kinetics of the same lesions embedded in147-mer Sp-modified DNA duplexes.	sp	66-68	nei like DNA glycosylase 1	Homo sapiens	241-246