PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26909952-7	2016	In addition, based on network analysis using the ingenuity pathway analysis software, DOX was found to suppress phosphorylation of extracellular signal-regulated kinase 1/2 and p38, suggesting that the mitogen-activated protein kinase signaling pathway plays a vital role in the anti-proliferative effect of DOX against RCC.	Docetaxel	86-89	mitogen-activated protein kinase 14	Homo sapiens	177-180	
35613826-12	2022	Mechanistically, DTX induced Ccl3 by relieving the inhibition of cAMP-response element binding protein on Ccl3 via reactive oxygen species accumulation, and Ccl3 then promoted proinflammatory macrophage polarization via activation of the Ccl3-C-C motif chemokine receptor 5-p38/interferon regulatory factor 5 pathway.	Docetaxel	17-20	mitogen-activated protein kinase 14	Homo sapiens	274-277	
27340870-0	2016	ST6Gal-I modulates docetaxel sensitivity in human hepatocarcinoma cells via the p38 MAPK/caspase pathway.	Docetaxel	19-28	mitogen-activated protein kinase 14	Homo sapiens	80-83	
27340870-6	2016	In addition, we found that p38 MAPK and caspase-3 inhibitors can reduce the enhanced apoptosis levels of MHCC97-H cells resulted by either ST6Gal-I silencing or docetaxel treatment.	Docetaxel	161-170	mitogen-activated protein kinase 14	Homo sapiens	27-30	
26909952-7	2016	In addition, based on network analysis using the ingenuity pathway analysis software, DOX was found to suppress phosphorylation of extracellular signal-regulated kinase 1/2 and p38, suggesting that the mitogen-activated protein kinase signaling pathway plays a vital role in the anti-proliferative effect of DOX against RCC.	Docetaxel	308-311	mitogen-activated protein kinase 14	Homo sapiens	177-180	
21968939-6	2012	Apoptosis in lenalidomide/docetaxel-treated cells was increased by 2.2-fold over single agent docetaxel and a corresponding increase in p53, p38, and BAD activation was observed in Western blots (P < 0.001).	Docetaxel	26-35	mitogen-activated protein kinase 14	Homo sapiens	141-144	
25231055-3	2014	Cell counting revealed significantly reduced cell growth during docetaxel treatment as a result of both activation of mitogen-activated protein kinase p38 (MAPK p38) and protein kinase D1 (PKD1), and, most importantly, the overexpression of the phosphorylation-mimicking mutant HSP27-3D.	Docetaxel	64-73	mitogen-activated protein kinase 14	Homo sapiens	151-154	
25231055-3	2014	Cell counting revealed significantly reduced cell growth during docetaxel treatment as a result of both activation of mitogen-activated protein kinase p38 (MAPK p38) and protein kinase D1 (PKD1), and, most importantly, the overexpression of the phosphorylation-mimicking mutant HSP27-3D.	Docetaxel	64-73	mitogen-activated protein kinase 14	Homo sapiens	161-164	
21656826-0	2011	Resistance to docetaxel-induced apoptosis in prostate cancer cells by p38/p53/p21 signaling.	Docetaxel	14-23	mitogen-activated protein kinase 14	Homo sapiens	70-73	
21656826-10	2011	Docetaxel increases p38 phosphorylation in LNCaP cells.	Docetaxel	0-9	mitogen-activated protein kinase 14	Homo sapiens	20-23	
21656826-11	2011	Treatment with p38-specific inhibitor SB203580 or knocking down p38 by siRNA significantly impaired the upregulation of p53 and p21 by docetaxel.	Docetaxel	135-144	mitogen-activated protein kinase 14	Homo sapiens	15-18	
21656826-11	2011	Treatment with p38-specific inhibitor SB203580 or knocking down p38 by siRNA significantly impaired the upregulation of p53 and p21 by docetaxel.	Docetaxel	135-144	mitogen-activated protein kinase 14	Homo sapiens	64-67	
21656826-12	2011	Knocking down p38 or p21 sensitizes LNCaP cells to docetaxel treatment and the antiapoptotic effect of p21 can be reversed by p38 siRNA in LNCaP cells.	Docetaxel	51-60	mitogen-activated protein kinase 14	Homo sapiens	14-17	
21656826-13	2011	CONCLUSIONS: Stimulation of the p38/p53/p21 signaling axis could be important for regulating the susceptibility towards docetaxel in prostate cancer.	Docetaxel	120-129	mitogen-activated protein kinase 14	Homo sapiens	32-35	
18158623-0	2008	Fibronectin-mediated activation of Akt2 protects human ovarian and breast cancer cells from docetaxel-induced apoptosis via inhibition of the p38 pathway.	Docetaxel	92-101	mitogen-activated protein kinase 14	Homo sapiens	142-145	
20527044-11	2010	The enhanced CMV promoter activity resulted from activation of p38 mitogen-activated protein kinase (MAPK) because inhibition of p38 MAPK blocked the docetaxel-induced increase in CMV promoter activity.	Docetaxel	150-159	mitogen-activated protein kinase 14	Homo sapiens	63-99	
18158623-4	2008	In the present study, we have investigated the role of the interaction between the Akt2/survivin survivial pathway and the ASK1/p38 apoptotic pathway in the phenomenon of resistance to docetaxel.	Docetaxel	185-194	mitogen-activated protein kinase 14	Homo sapiens	128-131	
18158623-6	2008	The activation of p38 kinase in response to docetaxel, on the other hand, is abolished by FN adhesion.	Docetaxel	44-53	mitogen-activated protein kinase 14	Homo sapiens	18-21	
18158623-8	2008	Our results indicate for the first time that p38 plays a critical role in FN adhesion-mediated resistance to docetaxel.	Docetaxel	109-118	mitogen-activated protein kinase 14	Homo sapiens	45-48