PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25550687-0	2014	CDK2-AP1 inhibits growth of breast cancer cells by regulating cell cycle and increasing docetaxel sensitivity in vivo and in vitro.	Docetaxel	88-97	cyclin dependent kinase 2	Homo sapiens	0-4	
25550687-13	2014	The data indicates that CDK2-AP1 can induce sensitivity to docetaxel treatment in breast cancer cells.	Docetaxel	59-68	cyclin dependent kinase 2	Homo sapiens	24-28	
20702488-8	2011	Antiproliferative effect after treatment with TXL was assessed by determination of the protein levels of p21, cyclinD1, PCNA, and cdk-2, which are the key regulators for cell cycle progression.	Docetaxel	46-49	cyclin dependent kinase 2	Homo sapiens	130-135	
21685708-5	2011	Docetaxel also decreased the expressions of cell cycle-related proteins, including cyclin-dependent kinase (CDK) 2, cyclin E, CDK4, cyclin D1, retinoblastoma protein, and proliferative cell nuclear antigen in PDGF-BB-stimulated VSMCs.	Docetaxel	0-9	cyclin dependent kinase 2	Homo sapiens	83-114	
18354084-6	2008	The CDK2 cytoplasmic redistribution is required for cell progression from S to G2-M phase, because the CDK2 T39A mutant, which lacks the phosphorylation site and is defective in cytoplasmic localization, severely affects cell cycle progression at the transition from S to G2-M. Interestingly, we also show that the Akt/CDK2 pathway is constitutively activated by some anticancer drugs, such as methotrexate and docetaxel, and under these conditions it promotes, rather than represses, cell death.	Docetaxel	411-420	cyclin dependent kinase 2	Homo sapiens	103-107	
18354084-6	2008	The CDK2 cytoplasmic redistribution is required for cell progression from S to G2-M phase, because the CDK2 T39A mutant, which lacks the phosphorylation site and is defective in cytoplasmic localization, severely affects cell cycle progression at the transition from S to G2-M. Interestingly, we also show that the Akt/CDK2 pathway is constitutively activated by some anticancer drugs, such as methotrexate and docetaxel, and under these conditions it promotes, rather than represses, cell death.	Docetaxel	411-420	cyclin dependent kinase 2	Homo sapiens	4-8	
18354084-6	2008	The CDK2 cytoplasmic redistribution is required for cell progression from S to G2-M phase, because the CDK2 T39A mutant, which lacks the phosphorylation site and is defective in cytoplasmic localization, severely affects cell cycle progression at the transition from S to G2-M. Interestingly, we also show that the Akt/CDK2 pathway is constitutively activated by some anticancer drugs, such as methotrexate and docetaxel, and under these conditions it promotes, rather than represses, cell death.	Docetaxel	411-420	cyclin dependent kinase 2	Homo sapiens	103-107