PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34389703-2	2021	Moreover, since RBM39 was identified as a target of sulfonamides, it has played a key role in the emerging field of molecule drug development.	Sulfonamides	52-64	RNA binding motif protein 39	Homo sapiens	16-21	
31686031-1	2020	The investigational drugs E7820, indisulam and tasisulam (aryl-sulfonamides) promote the degradation of the splicing factor RBM39 in a proteasome-dependent mechanism.	Sulfonamides	58-75	RNA binding motif protein 39	Homo sapiens	124-129	
31686031-5	2020	Our data demonstrate how aryl-sulfonamides neo-functionalize a shallow, non-conserved pocket on DCAF15 to selectively bind and degrade RBM39 and the closely related splicing factor RBM23 without the requirement for a high-affinity ligand, which has broad implications for the de novo discovery of molecular glue degraders.	Sulfonamides	25-42	RNA binding motif protein 39	Homo sapiens	135-140	
31693891-1	2019	Indisulam and related sulfonamides recruit the splicing factor RBM39 to the CRL4-DCAF15 E3 ubiquitin ligase, resulting in RBM39 ubiquitination and degradation.	Sulfonamides	22-34	RNA binding motif protein 39	Homo sapiens	63-68	
31693891-1	2019	Indisulam and related sulfonamides recruit the splicing factor RBM39 to the CRL4-DCAF15 E3 ubiquitin ligase, resulting in RBM39 ubiquitination and degradation.	Sulfonamides	22-34	RNA binding motif protein 39	Homo sapiens	122-127	
31693891-5	2019	RBM23, which is an RBM39 paralog, is also recruited to the CRL4-DCAF15 ligase through its RRM2 domain and undergoes sulfonamide-dependent degradation.	Sulfonamides	116-127	RNA binding motif protein 39	Homo sapiens	19-24	
31693911-0	2019	Structural Basis and Kinetic Pathway of RBM39 Recruitment to DCAF15 by a Sulfonamide Molecular Glue E7820.	Sulfonamides	73-84	RNA binding motif protein 39	Homo sapiens	40-45	
31693911-1	2019	E7820 and indisulam are two examples of aryl sulfonamides that recruit RBM39 to Rbx-Cul4-DDA1-DDB1-DCAF15 E3 ligase complex, leading to its ubiquitination and degradation by the proteasome.	Sulfonamides	40-57	RNA binding motif protein 39	Homo sapiens	71-76	
31693911-5	2019	The structural and kinetic studies confirm aryl sulfonamides as molecular glues in the recruitment of RBM39 and provide a framework for future efforts to utilize DCAF15 to degrade other proteins of interest.	Sulfonamides	43-60	RNA binding motif protein 39	Homo sapiens	102-107	
30889374-1	2019	A report in this issue of Cancer Cell identifies the RNA-binding protein RBM39 as a potential target in spliceosome mutant AML that can be targeted by existing sulfonamide drugs.	Sulfonamides	160-171	RNA binding motif protein 39	Homo sapiens	73-78	
28437394-0	2017	Selective degradation of splicing factor CAPERalpha by anticancer sulfonamides.	Sulfonamides	66-78	RNA binding motif protein 39	Homo sapiens	41-51	
28437394-3	2017	Here, we demonstrate that a series of anticancer sulfonamides NSC 719239 (E7820), indisulam, and NSC 339004 (chloroquinoxaline sulfonamide, CQS) induce proteasomal degradation of the U2AF-related splicing factor coactivator of activating protein-1 and estrogen receptors (CAPERalpha) via CRL4DCAF15 mediated ubiquitination in human cancer cell lines.	Sulfonamides	49-61	RNA binding motif protein 39	Homo sapiens	272-282	
28437394-3	2017	Here, we demonstrate that a series of anticancer sulfonamides NSC 719239 (E7820), indisulam, and NSC 339004 (chloroquinoxaline sulfonamide, CQS) induce proteasomal degradation of the U2AF-related splicing factor coactivator of activating protein-1 and estrogen receptors (CAPERalpha) via CRL4DCAF15 mediated ubiquitination in human cancer cell lines.	Sulfonamides	49-60	RNA binding motif protein 39	Homo sapiens	272-282	
28437394-4	2017	Both CRISPR-Cas9-based knockout of DCAF15 and a single amino acid substitution of CAPERalpha conferred resistance against sulfonamide-induced CAPERalpha degradation and cell-growth inhibition.	Sulfonamides	122-133	RNA binding motif protein 39	Homo sapiens	82-92	
28437394-4	2017	Both CRISPR-Cas9-based knockout of DCAF15 and a single amino acid substitution of CAPERalpha conferred resistance against sulfonamide-induced CAPERalpha degradation and cell-growth inhibition.	Sulfonamides	122-133	RNA binding motif protein 39	Homo sapiens	142-152	
28437394-5	2017	Thus, these sulfonamides represent selective chemical probes for disrupting CAPERalpha function and designate DCAFs as promising drug targets for promoting selective protein degradation in cancer therapy.	Sulfonamides	12-24	RNA binding motif protein 39	Homo sapiens	76-86	
28500024-0	2017	Anticancer Sulfonamides Induce Splicing Factor RBM39 Degradation.	Sulfonamides	11-23	RNA binding motif protein 39	Homo sapiens	47-52	
28500024-1	2017	Anticancer sulfonamides produce aberrant splicing by inducing degradation of the splicing factor RBM39.	Sulfonamides	11-23	RNA binding motif protein 39	Homo sapiens	97-102	
28302793-0	2017	Anticancer sulfonamides target splicing by inducing RBM39 degradation via recruitment to DCAF15.	Sulfonamides	11-23	RNA binding motif protein 39	Homo sapiens	52-57