PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
12615673-5	2003	We show that cathepsin H is expressed in atherosclerotic lesions in colocalization with E-LDL.	e-ldl	88-93	cathepsin H	Homo sapiens	13-24
15841317-3	2005	We studied the effect of E-LDL on the activation of plasminogen and matrix metalloproteinases (MMPs) in monocytes and vascular smooth muscle cells (VSMCs) as well as on MMP activation during cellular interactions.	e-ldl	25-30	matrix metallopeptidase 2	Homo sapiens	95-99
15841317-3	2005	We studied the effect of E-LDL on the activation of plasminogen and matrix metalloproteinases (MMPs) in monocytes and vascular smooth muscle cells (VSMCs) as well as on MMP activation during cellular interactions.	e-ldl	25-30	matrix metallopeptidase 2	Homo sapiens	95-98
15841317-5	2005	E-LDL in contrast to n-LDL induced substantial activation of the plasminogen activation system as well as of the MMP system in monocytic cells, as measured by enhanced cell surface expression of the urokinase receptor (uPAR),the extracellular matrix metalloproteinase Inducer (EMMPRIN) and the membrane type-1 MMPs (MT1-MMP,MMP-14), as well as by secretion of active uPA, and of MMP-9.	e-ldl	0-5	matrix metallopeptidase 2	Homo sapiens	113-116
15841317-5	2005	E-LDL in contrast to n-LDL induced substantial activation of the plasminogen activation system as well as of the MMP system in monocytic cells, as measured by enhanced cell surface expression of the urokinase receptor (uPAR),the extracellular matrix metalloproteinase Inducer (EMMPRIN) and the membrane type-1 MMPs (MT1-MMP,MMP-14), as well as by secretion of active uPA, and of MMP-9.	e-ldl	0-5	basigin (Ok blood group)	Homo sapiens	277-284
15841317-5	2005	E-LDL in contrast to n-LDL induced substantial activation of the plasminogen activation system as well as of the MMP system in monocytic cells, as measured by enhanced cell surface expression of the urokinase receptor (uPAR),the extracellular matrix metalloproteinase Inducer (EMMPRIN) and the membrane type-1 MMPs (MT1-MMP,MMP-14), as well as by secretion of active uPA, and of MMP-9.	e-ldl	0-5	matrix metallopeptidase 14	Homo sapiens	316-323
15841317-5	2005	E-LDL in contrast to n-LDL induced substantial activation of the plasminogen activation system as well as of the MMP system in monocytic cells, as measured by enhanced cell surface expression of the urokinase receptor (uPAR),the extracellular matrix metalloproteinase Inducer (EMMPRIN) and the membrane type-1 MMPs (MT1-MMP,MMP-14), as well as by secretion of active uPA, and of MMP-9.	e-ldl	0-5	matrix metallopeptidase 14	Homo sapiens	324-330
15841317-5	2005	E-LDL in contrast to n-LDL induced substantial activation of the plasminogen activation system as well as of the MMP system in monocytic cells, as measured by enhanced cell surface expression of the urokinase receptor (uPAR),the extracellular matrix metalloproteinase Inducer (EMMPRIN) and the membrane type-1 MMPs (MT1-MMP,MMP-14), as well as by secretion of active uPA, and of MMP-9.	e-ldl	0-5	plasminogen activator, urokinase	Homo sapiens	219-222
15841317-5	2005	E-LDL in contrast to n-LDL induced substantial activation of the plasminogen activation system as well as of the MMP system in monocytic cells, as measured by enhanced cell surface expression of the urokinase receptor (uPAR),the extracellular matrix metalloproteinase Inducer (EMMPRIN) and the membrane type-1 MMPs (MT1-MMP,MMP-14), as well as by secretion of active uPA, and of MMP-9.	e-ldl	0-5	matrix metallopeptidase 9	Homo sapiens	379-384
11676978-9	2001	CONCLUSIONS: These results show that E-LDL are potent inducers of egr-1 mRNA and may therefore represent a link between lipoproteins trapped in the subendothelium and enhanced expression of egr-1 in human atherosclerotic lesions.	e-ldl	37-42	early growth response 1	Homo sapiens	66-71
11676978-9	2001	CONCLUSIONS: These results show that E-LDL are potent inducers of egr-1 mRNA and may therefore represent a link between lipoproteins trapped in the subendothelium and enhanced expression of egr-1 in human atherosclerotic lesions.	e-ldl	37-42	early growth response 1	Homo sapiens	190-195
19146988-6	2009	As a consequence the uptake of E-LDL through type I and type II phagocytosis leads to increased lipid droplet formation and moderate upregulation of ABCA1 and ABCG1 while uptake of Ox-LDL leads to a rapid expansion of the lysosomal compartment and a pronounced upregulation of the ABCA1/ABCG1/AP-3 lipid efflux pathway.	e-ldl	31-36	ATP binding cassette subfamily A member 1	Homo sapiens	149-154
19146988-6	2009	As a consequence the uptake of E-LDL through type I and type II phagocytosis leads to increased lipid droplet formation and moderate upregulation of ABCA1 and ABCG1 while uptake of Ox-LDL leads to a rapid expansion of the lysosomal compartment and a pronounced upregulation of the ABCA1/ABCG1/AP-3 lipid efflux pathway.	e-ldl	31-36	ATP binding cassette subfamily G member 1	Homo sapiens	159-164
19146988-6	2009	As a consequence the uptake of E-LDL through type I and type II phagocytosis leads to increased lipid droplet formation and moderate upregulation of ABCA1 and ABCG1 while uptake of Ox-LDL leads to a rapid expansion of the lysosomal compartment and a pronounced upregulation of the ABCA1/ABCG1/AP-3 lipid efflux pathway.	e-ldl	31-36	ATP binding cassette subfamily A member 1	Homo sapiens	281-286
19146988-6	2009	As a consequence the uptake of E-LDL through type I and type II phagocytosis leads to increased lipid droplet formation and moderate upregulation of ABCA1 and ABCG1 while uptake of Ox-LDL leads to a rapid expansion of the lysosomal compartment and a pronounced upregulation of the ABCA1/ABCG1/AP-3 lipid efflux pathway.	e-ldl	31-36	ATP binding cassette subfamily G member 1	Homo sapiens	287-292
19132242-2	2008	Since nuclear factor-kappaB (NF-kappaB) is a major regulator of IL-8 transcription, we studied its activation in endothelial cells treated with E-LDL.	e-ldl	144-149	nuclear factor kappa B subunit 1	Homo sapiens	29-38
19132242-2	2008	Since nuclear factor-kappaB (NF-kappaB) is a major regulator of IL-8 transcription, we studied its activation in endothelial cells treated with E-LDL.	e-ldl	144-149	C-X-C motif chemokine ligand 8	Homo sapiens	64-68