PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	tanespimycin	79-91	checkpoint kinase 1	Homo sapiens	119-138	
25952464-4	2015	This phase II trial was designed to determine whether 17AAG could enhance the clinical activity of gemcitabine through degradation of Chk1 in patients with stage IV pancreatic cancer.	tanespimycin	54-59	checkpoint kinase 1	Homo sapiens	134-138	
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	tanespimycin	79-91	checkpoint kinase 1	Homo sapiens	140-144	
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	139-177	checkpoint kinase 1	Homo sapiens	16-20	
18927314-2	2008	We conducted a phase I study of irinotecan and the Hsp90 inhibitor 17AAG, which can also down-regulate Chk1, in patients with solid tumors.	tanespimycin	67-72	checkpoint kinase 1	Homo sapiens	103-107	
18927314-13	2008	Evidence for Hsp90 inhibition by 17AAG, resulting in phospho-Chk1 loss, abrogation of the G(2)-M cell cycle checkpoint, and cell death could be shown in tumor biopsy samples obtained at the MTD.	tanespimycin	33-38	checkpoint kinase 1	Homo sapiens	61-65	
15784732-2	2005	Recent results also demonstrated that Chk1 is depleted when cells are treated with heat shock protein 90 (Hsp90) inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	123-161	checkpoint kinase 1	Homo sapiens	38-42	
15699047-7	2005	Additional experiments demonstrated that the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin, which down-regulates Chk1, also sensitized a variety of human carcinoma cell lines to SN-38.	tanespimycin	61-99	checkpoint kinase 1	Homo sapiens	122-126	
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	139-177	checkpoint kinase 1	Homo sapiens	63-67	
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	179-185	checkpoint kinase 1	Homo sapiens	16-20	
14570880-3	2003	Consistent with Chk1 being an Hsp90 client, we also found that Chk1 but not Chk2 is destabilized in cells treated with the Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG).	tanespimycin	179-185	checkpoint kinase 1	Homo sapiens	63-67	
14570880-4	2003	17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells.	tanespimycin	0-6	checkpoint kinase 1	Homo sapiens	16-20	
14570880-4	2003	17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells.	tanespimycin	0-6	checkpoint kinase 1	Homo sapiens	49-53	
14570880-4	2003	17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells.	tanespimycin	0-6	checkpoint kinase 1	Homo sapiens	49-53	
14570880-4	2003	17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells.	tanespimycin	167-173	checkpoint kinase 1	Homo sapiens	16-20	
14570880-4	2003	17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells.	tanespimycin	167-173	checkpoint kinase 1	Homo sapiens	49-53	
14570880-4	2003	17-AAG-mediated Chk1 loss blocked the ability of Chk1 to target Cdc25A for proteolytic destruction, demonstrating that the Chk1 signaling pathway was disrupted in the 17-AAG-treated cells.	tanespimycin	167-173	checkpoint kinase 1	Homo sapiens	49-53	
14570880-5	2003	Finally, 17-AAG-mediated disruption of Chk1 activation dramatically sensitized various tumor cells to gemcitabine, an S phase-active chemotherapeutic agent.	tanespimycin	9-15	checkpoint kinase 1	Homo sapiens	39-43