PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
34272385-0	2021	Abraxas suppresses DNA end resection and limits break-induced replication by controlling SLX4/MUS81 chromatin loading in response to TOP1 inhibitor-induced DNA damage.	abraxas	0-7	SLX4 structure-specific endonuclease subunit	Homo sapiens	89-93
27131364-3	2016	Here, we report that functioning of SLX4 is dependent on its dimerization via an oligomerization motif called the BTB domain.	btb	114-117	SLX4 structure-specific endonuclease subunit	Homo sapiens	36-40
33596761-4	2021	Recently, SLX4 was shown to interact with MutSbeta, a heterodimeric protein involved in DNA mismatch repair, trinucleotide repeat instability, crosslink repair and recombination.	trinucleotide	109-122	SLX4 structure-specific endonuclease subunit	Homo sapiens	10-14
33596761-8	2021	Furthermore, we speculate that MutSbeta and SLX4 may provide an alternative cellular mechanism that modulates trinucleotide instability.	trinucleotide	110-123	SLX4 structure-specific endonuclease subunit	Homo sapiens	44-48
32636717-11	2020	Similarly, increased frequency of tryptic phosphopeptides were observed from POM121C, SCN8A, TMED8, NSUN7, SLX4, MADD, DNLZ, PDE3B, UTY, DEPDC7, MTX1, MYO1E, RXRB, SYDE1, FN1, PUS7L, FYCO1, USP26, ACAP2, AHI1, KSR2, LMAN1, ZNF280D and SLC8A2 amongst others.	Phosphopeptides	42-57	SLX4 structure-specific endonuclease subunit	Homo sapiens	107-111
28257701-4	2017	Within SMX, SLX4 co-ordinates the SLX1 and MUS81-EME1 nucleases for Holliday junction resolution, in a reaction stimulated by XPF-ERCC1.	Sulfamethoxazole	7-10	SLX4 structure-specific endonuclease subunit	Homo sapiens	12-16
27131364-5	2016	Disruption of BTB dimerization abrogates nuclear foci formation and telomeric localization of not only SLX4 but also of its associated nucleases.	btb	14-17	SLX4 structure-specific endonuclease subunit	Homo sapiens	103-107
27131364-6	2016	Furthermore, dimerization-deficient SLX4 mutants cause defective cellular response to DNA interstrand crosslinking agent and telomere maintenance, underscoring the contribution of BTB domain-mediated dimerization of SLX4 in genome and telomere maintenance.	btb	180-183	SLX4 structure-specific endonuclease subunit	Homo sapiens	36-40
27131364-6	2016	Furthermore, dimerization-deficient SLX4 mutants cause defective cellular response to DNA interstrand crosslinking agent and telomere maintenance, underscoring the contribution of BTB domain-mediated dimerization of SLX4 in genome and telomere maintenance.	btb	180-183	SLX4 structure-specific endonuclease subunit	Homo sapiens	216-220
23840564-7	2013	While wild type SLX4 and all the other variants fully rescued the sensitivity to mitomycin C (MMC), campthothecin (CPT), and PARP inhibitor (Olaparib) the p.W823* SLX4 mutant failed to do so.	olaparib	141-149	SLX4 structure-specific endonuclease subunit	Homo sapiens	163-167
25533185-4	2015	The SIMs of SLX4 are dispensable for ICL repair but important for processing CPT-induced replication intermediates, suppressing fragile site instability, and localizing SLX4 to ALT telomeres.	cpt	77-80	SLX4 structure-specific endonuclease subunit	Homo sapiens	12-16
23840564-7	2013	While wild type SLX4 and all the other variants fully rescued the sensitivity to mitomycin C (MMC), campthothecin (CPT), and PARP inhibitor (Olaparib) the p.W823* SLX4 mutant failed to do so.	Mitomycin	81-92	SLX4 structure-specific endonuclease subunit	Homo sapiens	16-20
23840564-7	2013	While wild type SLX4 and all the other variants fully rescued the sensitivity to mitomycin C (MMC), campthothecin (CPT), and PARP inhibitor (Olaparib) the p.W823* SLX4 mutant failed to do so.	Mitomycin	94-97	SLX4 structure-specific endonuclease subunit	Homo sapiens	16-20
25758781-7	2015	Depletion and complementation experiments validated the causal relationship between SLX4 defects and sensitivity to raltitrexed and cytarabine in addition to camptothecin.	raltitrexed	116-127	SLX4 structure-specific endonuclease subunit	Homo sapiens	84-88
25758781-7	2015	Depletion and complementation experiments validated the causal relationship between SLX4 defects and sensitivity to raltitrexed and cytarabine in addition to camptothecin.	Cytarabine	132-142	SLX4 structure-specific endonuclease subunit	Homo sapiens	84-88
24794496-3	2014	Here, we show that human SLX4 is recruited to sites of ICL induction but that the UBZ-deleted form of SLX4 in cells from FA patients is not.	(2s)-2-({n-[(R)-({[(Benzyloxy)carbonyl]amino}methyl)(Hydroxy)phosphoryl]-L-Leucyl}amino)butanoic Acid	82-85	SLX4 structure-specific endonuclease subunit	Homo sapiens	102-106
24794496-5	2014	We show that the first (UBZ-1) but not the second UBZ domain of SLX4 binds to ubiquitin polymers, with a preference for K63-linked chains.	ubiquitin polymers	78-96	SLX4 structure-specific endonuclease subunit	Homo sapiens	64-68
21314952-10	2011	RESULTS: 43 SNPs were found significantly associated (FDR<0.005) with paclitaxel response, with 10 belonging to protein-coding genes (CFTR, ROBO1, PTPRD, BTBD12, DCT, SNTG1, SGCD, LPHN2, GRIK1, ZNF607).	Paclitaxel	73-83	SLX4 structure-specific endonuclease subunit	Homo sapiens	157-163
23840564-7	2013	While wild type SLX4 and all the other variants fully rescued the sensitivity to mitomycin C (MMC), campthothecin (CPT), and PARP inhibitor (Olaparib) the p.W823* SLX4 mutant failed to do so.	campthothecin	100-113	SLX4 structure-specific endonuclease subunit	Homo sapiens	16-20
23840564-7	2013	While wild type SLX4 and all the other variants fully rescued the sensitivity to mitomycin C (MMC), campthothecin (CPT), and PARP inhibitor (Olaparib) the p.W823* SLX4 mutant failed to do so.	olaparib	141-149	SLX4 structure-specific endonuclease subunit	Homo sapiens	16-20
20670884-2	2010	(2010) show that Mec1 (hATR) promotes the association of Slx4 and Rtt107 with Dpb11 (hTopBP1) in response to MMS-induced DNA alkylation, suggesting that Slx4 and Rtt107 might coordinate repair factors specifically at damaged replication forks.	Methyl Methanesulfonate	109-112	SLX4 structure-specific endonuclease subunit	Homo sapiens	57-61
20670884-2	2010	(2010) show that Mec1 (hATR) promotes the association of Slx4 and Rtt107 with Dpb11 (hTopBP1) in response to MMS-induced DNA alkylation, suggesting that Slx4 and Rtt107 might coordinate repair factors specifically at damaged replication forks.	Methyl Methanesulfonate	109-112	SLX4 structure-specific endonuclease subunit	Homo sapiens	153-157
19595721-7	2009	Depletion of SLX4 causes a decrease in DSB-induced homologous recombination.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	39-42	SLX4 structure-specific endonuclease subunit	Homo sapiens	13-17
19596235-4	2009	Depletion of SLX4 causes sensitivity to mitomycin C and camptothecin and reduces the efficiency of DSB repair in vivo.	Mitomycin	40-51	SLX4 structure-specific endonuclease subunit	Homo sapiens	13-17
19596235-4	2009	Depletion of SLX4 causes sensitivity to mitomycin C and camptothecin and reduces the efficiency of DSB repair in vivo.	Camptothecin	56-68	SLX4 structure-specific endonuclease subunit	Homo sapiens	13-17
19596236-6	2009	Depletion of SLX1 and SLX4 results in 53BP1 foci accumulation and H2AX phosphorylation as well as cellular hypersensitivity to MMS.	Methyl Methanesulfonate	127-130	SLX4 structure-specific endonuclease subunit	Homo sapiens	22-26