PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34331013-5	2021	Because addition of the BCL2 inhibitor venetoclax resulted in compensatory upregulation of MCL1, we established a three-drug combination composed of sirolimus, venetoclax, and the MCL1 inhibitor S63845.	Sirolimus	149-158	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	91-95	
26452980-6	2015	Notably, INK128 was more potent than the TORC1 inhibitor rapamycin in down-regulating Mcl-1, diminishing AKT and 4EBP1 phosphorylation, and potentiating ABT-737 activity.	Sirolimus	57-66	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	86-91	
28186963-7	2017	In addition, B392 enhanced the cytotoxicity of sirolimus in sirolimus-resistant acute leukemic cells through inhibition of Akt/mTOR pathway and Mcl-1 protein expression, and also was active in the p-glycoprotein (p-gp)-overexpressing National Cancer Institute/Adriamycin-Resistant cells with little susceptibility to p-gp.	Sirolimus	47-56	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	144-149	
32062191-3	2020	Here we found that rapamycin inhibited human soluble BAFF (hsBAFF)-stimulated cell proliferation by inducing G1-cell cycle arrest, which was through downregulating the protein levels of CDK2, CDK4, CDK6, cyclin A, cyclin D1, and cyclin E. Rapamycin reduced hsBAFF-stimulated cell survival by downregulating the levels of anti-apoptotic proteins (Mcl-1, Bcl-2, Bcl-xL and survivin) and meanwhile upregulating the levels of pro-apoptotic proteins (BAK and BAX).	Sirolimus	19-28	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	346-351	
23580240-0	2013	Concurrent inhibition of PI3K and mTORC1/mTORC2 overcomes resistance to rapamycin induced apoptosis by down-regulation of Mcl-1 in mantle cell lymphoma.	Sirolimus	72-81	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	122-127	
25780003-4	2015	Mcl-1 expression intensity in NMSC was decreased in tacrolimus-treated patients compared with sirolimus-treated patients and the nonimmunosuppressed population (P = .024).	Sirolimus	94-103	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-5	
25780003-7	2015	Importantly in NMSC, Bcl-xL expression was reduced with immunosuppression exposure, and Mcl-1 expression was reduced in tacrolimus-treated compared with sirolimus-treated patients.	Sirolimus	153-162	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	88-93	
23741975-4	2014	Combined treatment with rapamycin and IDA down-regulated Bcl-2 and Mcl-1, and inhibited the activation of phosphoinositide 3-kinase (PI3K)/mTOR and extracellular signal-related kinase (ERK).	Sirolimus	24-33	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	67-72	
23580240-9	2013	While Mcl-1 protein levels remained unchanged after coculture with rapamycin, they were down-regulated in NVP-BEZ235 treated cells.	Sirolimus	67-76	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	6-11	
17010674-4	2006	We tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells and found that it sensitized to GC-induced apoptosis via modulation of antiapoptotic MCL1.	Sirolimus	30-39	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	182-186	
22190165-11	2012	Sorafenib/rapamycin combination resulted in downregulation of pAkt, pmTOR, p-p70S6K, p4EBP1, pGSK3beta, Mcl1, and Bcl-Xl.	Sirolimus	10-19	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	104-108	
21083937-12	2010	Rapamycin enhanced GC-induced apoptosis and this was not achieved by modulation of glucocorticoid receptor (GR) expression, but synergistically up-regulation of pro-apoptotic proteins like caspase-3, Bax, and Bim, and down-regulation of anti-apoptotic protein of Mcl-1.	Sirolimus	0-9	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	263-268