PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23185512-4	2012	CCL2-mediated VCAM-1 expression was attenuated by CCR2 inhibitor (RS102895), PKCdelta inhibitor (rottlerin), p38MAPK inhibitor (SB203580), and AP-1 inhibitors (curcumin and tanshinone IIA).	SB 203580	128-136	vascular cell adhesion molecule 1	Homo sapiens	14-20	
22210380-8	2012	Interestingly, CORM-3 inhibited MAPK p38, and the p38 inhibitor SB203580 downregulated VCAM-1 expression.	SB 203580	64-72	vascular cell adhesion molecule 1	Homo sapiens	87-93	
27122190-5	2016	In addition, the nuclear factor-kappaB (NF-kappaB) inhibitor, Bay 11-7082, and mitogen-activated protein kinase (MAPK) inhibitors (SB203580 and U0126) respectively reduced the adhesion of monocytes to TNF-alpha-stimulated HUVECs, and suppressed ICAM-1 and VCAM-1 expression in TNF-alpha stimulated HUVECs.	SB 203580	131-139	vascular cell adhesion molecule 1	Homo sapiens	256-262	
23709128-9	2013	In the meantime, both RHL and p38 inhibitor (SB203580) inhibited phosphorylation of p38 and mitogen-activated protein kinase-activated protein kinase-2 (MAPKAPK-2) and transcription and expression of ICAM-1 and VCAM-1.	SB 203580	45-53	vascular cell adhesion molecule 1	Homo sapiens	211-217	
22122523-7	2012	In addition, the p38 MAPK inhibitor (SB 203580) significantly attenuated Pg LPS-induced VCAM-1 expression.	SB 203580	37-46	vascular cell adhesion molecule 1	Homo sapiens	88-94	
17982268-10	2007	In contrast, SB203580, an inhibitor of p38 MAPK inhibited both the Ang II-induced enrichment of ICAM-1 and VCAM-1.	SB 203580	13-21	vascular cell adhesion molecule 1	Homo sapiens	107-113	
18613029-4	2008	Our initial data indicated that blockade of p38 activity by chemical inhibitor SB203580 (SB) at 10 microM moderately inhibited TNF-alpha-induced expression of three types of CAMs; ICAM-1, VCAM-1 and E-selectin, indicating that p38 may be involved in the process.	SB 203580	79-87	vascular cell adhesion molecule 1	Homo sapiens	188-194	
18613029-10	2008	The inhibition of SB at 10 microM on TNF-alpha-induced ICAM-1, VCAM-1 and E-selectin is likely due to the nonspecific effect of SB.	SB 203580	18-20	vascular cell adhesion molecule 1	Homo sapiens	63-69	
18032781-4	2008	The enhancement of VCAM-1 expression caused by U46619 occurred at the transcriptional level and was inhibited either by SP600125, a c-Jun N-terminal kinase (JNK) inhibitor, or by overexpression of a dominant-negative JNK1, but not by SB203580, a p38 mitogen-activated protein kinase inhibitor.	SB 203580	234-242	vascular cell adhesion molecule 1	Homo sapiens	19-25	
17880767-6	2007	The p38 mitogen activated protein(MAP) kinase inhibitors SB203580 and SB202190, and partially the c-Jun NH2-terminal kinase (JNK) inhibitor SP600127, decreased insulin effect on VCAM-1.	SB 203580	57-65	vascular cell adhesion molecule 1	Homo sapiens	178-184	
16644474-6	2006	Moreover, calcium chelator BAPTA, ERK1/2 inhibitor PD98059, p38 inhibitor SB203580 significantly reduced the production of nicotine-activated surface/soluble VCAM-1 and E-selectin and both of the remained levels were no longer regulated by estrogen.	SB 203580	74-82	vascular cell adhesion molecule 1	Homo sapiens	158-164	
16480622-9	2005	The VCAM-1 content in the supernatant of BS group (125 +/- 10 ng/L) was obviously higher than that in NC (23 +/- 3 ng/L), SB203580 (27 +/- 5 ng/L) and PDTC (29 +/- 5 ng/L) groups.	SB 203580	122-130	vascular cell adhesion molecule 1	Homo sapiens	4-10	
15805138-6	2005	HIV-1 Tat protein-induced VCAM-1 expression was abolished by the NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) and the p38 MAPK inhibitor SB-203580.	SB 203580	147-156	vascular cell adhesion molecule 1	Homo sapiens	26-32	
15805138-8	2005	Similarly to VCAM-1 expression, HIV-1 Tat protein-induced NF-kappaB activation and ROS generation were abrogated by PDTC and SB-203580.	SB 203580	125-134	vascular cell adhesion molecule 1	Homo sapiens	13-19