PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
34395412-4	2021	In vitro, Jam3 expression varies along airway basal stem cell (BSC) differentiation and upon DAPT treatment or IL6 exposure.	dapt	93-97	junction adhesion molecule 3	Mus musculus	10-14
34464887-15	2021	Moreover, pravastatin up-regulated the levels of junction proteins ZO-1, JAM-C, and VE-Cadherin.	Pravastatin	10-21	junction adhesion molecule 3	Mus musculus	73-78
30148763-14	2019	NE expression was upregulated, whereas JAM-C expression was downregulated in the lungs after CLP or rmCIRP administration.	rmcirp	100-106	junction adhesion molecule 3	Mus musculus	39-44
17116731-3	2006	As opposed to macrovascular endothelial cells that constitutively expressed JAM-C in cell-cell contacts, in quiescent microvascular endothelial cells, JAM-C localized mainly intracellularly, and was recruited to junctions upon short-term stimulation with vascular endothelial growth factor (VEGF) or histamine.	Histamine	300-309	junction adhesion molecule 3	Mus musculus	151-156
15485832-6	2004	In vivo, inhibition of JAM-C with soluble mouse JAM-C resulted in a 50% reduction of neutrophil emigration in the mouse model of acute thioglycollate-induced peritonitis.	Thioglycolates	135-149	junction adhesion molecule 3	Mus musculus	23-28
15485832-6	2004	In vivo, inhibition of JAM-C with soluble mouse JAM-C resulted in a 50% reduction of neutrophil emigration in the mouse model of acute thioglycollate-induced peritonitis.	Thioglycolates	135-149	junction adhesion molecule 3	Mus musculus	48-53
28192890-2	2017	In this study, we tested the effects of a JAM-C blocking antibody on the resolution of kidney injuries and inflammation in a mouse model of cisplatin-induced acute kidney injury (AKI).	Cisplatin	140-149	junction adhesion molecule 3	Mus musculus	42-47
28192890-6	2017	Treatment with a JAM-C blocking antibody on days 4 and 5 promoted the functional and histologic recovery of cisplatin-induced AKI on days 5 and 6.	Cisplatin	108-117	junction adhesion molecule 3	Mus musculus	17-22
28192890-8	2017	CONCLUSIONS: These results demonstrated that reverse TEM is involved in the resolution of neutrophilic inflammation in cisplatin-induced AKI and that JAM-C is an important regulator of this process.	Cisplatin	119-128	junction adhesion molecule 3	Mus musculus	150-155
26047922-3	2015	Here we demonstrate that the lipid chemoattractant leukotriene B4 (LTB4) was efficacious at causing loss of venular JAM-C and promoting neutrophil reverse transendothelial cell migration (rTEM) in vivo.	Leukotriene B4	51-65	junction adhesion molecule 3	Mus musculus	116-121
23372751-4	2013	Blocking of JAM-C efficiently attenuated cerulean-induced pancreatitis, rheumatoid arthritis or inflammation induced by ischemia and reperfusion in mice.	cerulean	41-49	junction adhesion molecule 3	Mus musculus	12-17
16767690-7	2006	Conversely, cerulein-induced acute pancreatitis was more severe in transgenic mice overexpressing JAM-C on endothelial cells under the control of the Tie2 promoter.	Ceruletide	12-20	junction adhesion molecule 3	Mus musculus	98-103