PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
11772950-4	2002	Angiostatin blocked chemotaxis of neutrophils to CXCR2 chemokine receptor agonists (IL-8, MIP-2, and GROalpha), formyl-Met-Leu-Phe (fMLP), and 12-O-tetradecanoylphorbol 13-acetate, and repressed fMLP-induced mitochondrial activity.	N-Formylmethionine Leucyl-Phenylalanine	112-130	plasminogen	Mus musculus	0-11
12577239-1	2002	The effects of dose per fraction on the ability of amifostine exposure to elevate angiostatin levels in the serum of mice and to inhibit spontaneous metastases formation using the well-characterized murine Sa-NH sarcoma were investigated.	Amifostine	51-61	plasminogen	Mus musculus	82-93
12577239-8	2002	The effects of amifostine exposure on serum levels of the angiogenesis inhibitor angiostatin were also determined using Western analysis.	Amifostine	15-25	plasminogen	Mus musculus	81-92
12577239-9	2002	Correlating with the antimetastatic effect measured, exposure of animals to 50 mg/kg of amifostine resulted in a four-fold enhanced serum level of angiostatin above control levels.	Amifostine	88-98	plasminogen	Mus musculus	147-158
12577239-13	2002	While the dose responses for angiostatin production and metastases inhibition by amifostine are well correlated, the precise mechanism of action underlying these phenomena is unclear but is suggestive of a redox driven process(es).	Amifostine	81-91	plasminogen	Mus musculus	29-40
12417566-7	2002	In a thioglycollate model of peritoneal inflammation, leukocyte migration at 72 hours increased significantly in Plg(+/-)/pCPB(+/-) and Plg(+/-)/pCPB(-/-) compared with their wild-type counterparts.	Thioglycolates	5-19	plasminogen	Mus musculus	113-116
12417566-7	2002	In a thioglycollate model of peritoneal inflammation, leukocyte migration at 72 hours increased significantly in Plg(+/-)/pCPB(+/-) and Plg(+/-)/pCPB(-/-) compared with their wild-type counterparts.	Thioglycolates	5-19	plasminogen	Mus musculus	136-139
12417566-8	2002	These studies demonstrate a definitive role of pCPB as a modulator of the pivotal functions of Plg in fibrinolysis and cell migration in vivo.	Polychlorinated Biphenyls	47-51	plasminogen	Mus musculus	95-98
12213719-4	2002	We report successful treatment of endometriosis in estrogen-supplemented ovariectomized mice by transient overexpression (6 to 10 days of duration) of the gene for a natural angiogenesis inhibitor angiostatin, delivered to the peritoneum by a replication-deficient adenovirus vector (AdAngiostatin).	adangiostatin	284-297	plasminogen	Mus musculus	197-208
12883524-3	2003	Poly(D-L-lactide-co-glycolide) (PLG) is a biodegradable and biocompatible polymer that has been used to encapsulate plasmid DNA.	Polylactic Acid-Polyglycolic Acid Copolymer	0-30	plasminogen	Mus musculus	32-35
12883524-3	2003	Poly(D-L-lactide-co-glycolide) (PLG) is a biodegradable and biocompatible polymer that has been used to encapsulate plasmid DNA.	Polymers	74-81	plasminogen	Mus musculus	32-35
12885346-4	2003	These cells are protected from graft rejection in alginate microcapsules to function as "micro-organs" to deliver angiostatin in vivo.	Alginates	50-58	plasminogen	Mus musculus	114-125
12657615-8	2003	CONCLUSIONS: Together with previous work done by the authors, this study indicates that choroidal neovascularization is extremely sensitive to the modulation of Plg/PA system activity.	Protactinium	165-167	plasminogen	Mus musculus	161-164
12225871-4	2002	The results indicated that Plg mRNA was undetectable in the normal brain, but after kainate injection it was induced in neuronal cells in multiple, but specific areas, including layers II-III of the neocortex; the olfactory bulb, anterior olfactory nucleus, and the piriform cortex; the caudate/putamen and accumbens nucleus shell; throughout the amygdaloid complex; and in the CAI/CA3 subfields of the hippocampus.	Kainic Acid	84-91	plasminogen	Mus musculus	27-30
11772950-4	2002	Angiostatin blocked chemotaxis of neutrophils to CXCR2 chemokine receptor agonists (IL-8, MIP-2, and GROalpha), formyl-Met-Leu-Phe (fMLP), and 12-O-tetradecanoylphorbol 13-acetate, and repressed fMLP-induced mitochondrial activity.	Tetradecanoylphorbol Acetate	143-179	plasminogen	Mus musculus	0-11
11389115-2	2001	In this study, Poly (DL-lactide-co-glycolide) (PLG) microparticles containing a combination of isoniazid and rifampicin were developed as sustained release carrier systems.	poly (dl-lactide-co-glycolide)	15-45	plasminogen	Mus musculus	47-50
11726640-13	2001	CONCLUSIONS: Angiostatin inhibits oxygen-induced intravitreal pathologic retinal angiogenesis without affecting the development of physiological retinal vascularization, development, and growth of newborn mice.	Oxygen	34-40	plasminogen	Mus musculus	13-24
11774255-8	2002	The effect of amifostine exposure on serum levels of the angiogenesis inhibitor angiostatin was also determined using Western blot analysis.	Amifostine	14-24	plasminogen	Mus musculus	80-91
11774255-9	2002	Consistent with the antimetastatic effect, exposure of animals to 50 mg/kg of amifostine resulted in a 4-fold enhanced serum level of angiostatin above control levels.	Amifostine	78-88	plasminogen	Mus musculus	134-145
11774255-17	2002	The abilities of amifostine and its active thiol WR-1065 to stimulate angiostatin production in mice, and to inhibit the MMP enzymatic activities and invasion ability of Sa-NH cells under in vitro conditions, are consistent with the observed antimetastatic effects exhibited against Sa-NH tumors growing in vivo.	Amifostine	17-27	plasminogen	Mus musculus	70-81
11733368-2	2001	On gross examination, we found that Plg(0) livers became enlarged and pale with foci of red nodules as early as 4 weeks after CCl(4) injection, while Plg(+) livers appeared minimally affected by 6 weeks.	Cefaclor	126-129	plasminogen	Mus musculus	36-39
11717653-2	2001	STUDY DESIGN: Inactivated GBS antigen was microencapsulated in poly (D, L-lactic-co-glycolic acid) (PLG) with a water-in-oil-in-water double emulsion technique.	Polylactic Acid-Polyglycolic Acid Copolymer	63-98	plasminogen	Mus musculus	100-103
11717653-2	2001	STUDY DESIGN: Inactivated GBS antigen was microencapsulated in poly (D, L-lactic-co-glycolic acid) (PLG) with a water-in-oil-in-water double emulsion technique.	Water	112-117	plasminogen	Mus musculus	100-103
11717653-2	2001	STUDY DESIGN: Inactivated GBS antigen was microencapsulated in poly (D, L-lactic-co-glycolic acid) (PLG) with a water-in-oil-in-water double emulsion technique.	Oils	121-124	plasminogen	Mus musculus	100-103
11717653-2	2001	STUDY DESIGN: Inactivated GBS antigen was microencapsulated in poly (D, L-lactic-co-glycolic acid) (PLG) with a water-in-oil-in-water double emulsion technique.	Water	128-133	plasminogen	Mus musculus	100-103
11389115-2	2001	In this study, Poly (DL-lactide-co-glycolide) (PLG) microparticles containing a combination of isoniazid and rifampicin were developed as sustained release carrier systems.	Isoniazid	95-104	plasminogen	Mus musculus	47-50
11389115-2	2001	In this study, Poly (DL-lactide-co-glycolide) (PLG) microparticles containing a combination of isoniazid and rifampicin were developed as sustained release carrier systems.	Rifampin	109-119	plasminogen	Mus musculus	47-50
11389115-3	2001	A single dose of PLG microparticles exhibited a sustained release of isoniazid and rifampicin in vivo up to 7 and 6 weeks, respectively.	Isoniazid	69-78	plasminogen	Mus musculus	17-20
11389115-3	2001	A single dose of PLG microparticles exhibited a sustained release of isoniazid and rifampicin in vivo up to 7 and 6 weeks, respectively.	Rifampin	83-93	plasminogen	Mus musculus	17-20
11287327-3	2001	Acute exposure to angiostatin or endostatin nearly abolished subsequent endothelial [Ca(2+)](i) responses to carbachol or to thapsigargin; conversely, thapsigargin attenuated the Ca(2+) signal elicited by endostatin.	Carbachol	109-118	plasminogen	Mus musculus	18-29
11287327-3	2001	Acute exposure to angiostatin or endostatin nearly abolished subsequent endothelial [Ca(2+)](i) responses to carbachol or to thapsigargin; conversely, thapsigargin attenuated the Ca(2+) signal elicited by endostatin.	Thapsigargin	125-137	plasminogen	Mus musculus	18-29
11287327-3	2001	Acute exposure to angiostatin or endostatin nearly abolished subsequent endothelial [Ca(2+)](i) responses to carbachol or to thapsigargin; conversely, thapsigargin attenuated the Ca(2+) signal elicited by endostatin.	Thapsigargin	151-163	plasminogen	Mus musculus	18-29
10438065-0	1999	PLG microparticles stabilised using enteric coating polymers as oral vaccine delivery systems.	Polymers	52-60	plasminogen	Mus musculus	0-3
10743633-6	2000	In addition, PDGF-BB has been shown to modulate chondrogensis by resting zone cells implanted in poly(D,L-lactide-co-glycolide) (PLG) scaffolds.	Polylactic Acid-Polyglycolic Acid Copolymer	97-126	plasminogen	Mus musculus	129-132
11231576-4	2001	PKal, which is inhibited by ecotin, is required for adipose conversion, Plg activation and 3T3-L1 differentiation.	ecotin	28-34	plasminogen	Mus musculus	72-75
9490683-3	1998	To directly characterize plasminogen"s involvement in the inflammatory response, we used thioglycollate to induce a peritoneal inflammatory reaction in Plg(+/+), Plg(+/-), and Plg(-/-) mice.	Thioglycolates	89-103	plasminogen	Mus musculus	152-155
10050071-5	1999	Dephosphorylation of ERK and other tyrosine-phosphorylated proteins was blocked by pretreatment of the cells with sodium meta-vanadate, an inhibitor of protein tyrosine phosphatases, indicating that angiostatin signaling may require the activity of a tyrosine phosphatase.	Tyrosine	35-43	plasminogen	Mus musculus	199-210
10050071-5	1999	Dephosphorylation of ERK and other tyrosine-phosphorylated proteins was blocked by pretreatment of the cells with sodium meta-vanadate, an inhibitor of protein tyrosine phosphatases, indicating that angiostatin signaling may require the activity of a tyrosine phosphatase.	Vanadates	114-134	plasminogen	Mus musculus	199-210
9813061-5	1998	Utilizing murine RAW264.7 macrophages and thioglycollate-elicited peritoneal macrophages, we demonstrate that angiostatin-like fragments are generated as a byproduct of the proteolytic regulation of membrane-bound plasmin.	Thioglycolates	42-56	plasminogen	Mus musculus	110-121
9813061-10	1998	Lavage fluid recovered from the peritoneal cavities of mice previously injected with thioglycollate contained angiostatin-like plasmin fragments similar to those generated in vitro.	Thioglycolates	85-99	plasminogen	Mus musculus	110-121
9657317-2	1998	Mice immunized with 71-kDa microparticles entrapped in DL-PLG (PLG-MPs) exhibited significantly higher T-cell stimulation and cytokine release in comparison to 71-kDa emulsified in Freund"s incomplete adjuvant (FIA) as well as a BCG vaccinated group throughout the post-immunization (p.im.)	KDA	23-26	plasminogen	Mus musculus	58-61
9657317-2	1998	Mice immunized with 71-kDa microparticles entrapped in DL-PLG (PLG-MPs) exhibited significantly higher T-cell stimulation and cytokine release in comparison to 71-kDa emulsified in Freund"s incomplete adjuvant (FIA) as well as a BCG vaccinated group throughout the post-immunization (p.im.)	KDA	23-26	plasminogen	Mus musculus	63-66
9657317-2	1998	Mice immunized with 71-kDa microparticles entrapped in DL-PLG (PLG-MPs) exhibited significantly higher T-cell stimulation and cytokine release in comparison to 71-kDa emulsified in Freund"s incomplete adjuvant (FIA) as well as a BCG vaccinated group throughout the post-immunization (p.im.)	71-kda	20-26	plasminogen	Mus musculus	58-61
9657317-2	1998	Mice immunized with 71-kDa microparticles entrapped in DL-PLG (PLG-MPs) exhibited significantly higher T-cell stimulation and cytokine release in comparison to 71-kDa emulsified in Freund"s incomplete adjuvant (FIA) as well as a BCG vaccinated group throughout the post-immunization (p.im.)	71-kda	20-26	plasminogen	Mus musculus	63-66
9245707-4	1997	Recombinant murine angiostatin was purified from the culture medium of angiostatin baculovirus-infected insect cells (yield = 1 mg/liter) with a single-step of lysine-Sepharose chromatography.	Lysine	160-166	plasminogen	Mus musculus	19-30
23100908-1	1997	A 71 kDa cell wall associated protein ofM.tuberculosis H(37)Ra, on encapsulation in biodegradable microparticles composed of poly-DL-lactide-co-glycolide (DL-PLG) exhibited higher level of T-cell stimulation and cytokine release as compared to 71 kDa-FIA in mice as evaluated till sixteenth week post immunization (p.im.).	poly-dl-lactide-co-glycolide	125-153	plasminogen	Mus musculus	158-161
9328577-1	1997	A synthetic peptide representing a measles virus (MV) cytotoxic T cell epitope (CTL) when encapsulated in poly (D,L-lactide co-glycolide) (PLG) 50:50 microparticles induced a strong CTL response after a single intraperitoneal immunization of mice which was greater than that following administration of the peptide in Freund"s complete adjuvant.	Polylactic Acid-Polyglycolic Acid Copolymer	106-137	plasminogen	Mus musculus	139-142
9245707-4	1997	Recombinant murine angiostatin was purified from the culture medium of angiostatin baculovirus-infected insect cells (yield = 1 mg/liter) with a single-step of lysine-Sepharose chromatography.	Sepharose	167-176	plasminogen	Mus musculus	19-30
9157597-3	1997	Plasminogen activation was markedly reduced by addition of amiloride or of anti-murine u-PA antibodies but not by addition of anti-murine t-PA antibodies, and it was not stimulated by addition of fibrin.	Amiloride	59-68	plasminogen	Mus musculus	0-11
9038287-2	1997	We tested the protective immunity elicited by intragastric vaccination with phosphorylcholine (PC) encapsulated in poly(DL-lactide-co-glycolide) (DL-PLG) microspheres against Salmonella typhimurium in a mouse model of invasive intestinal infection.	Phosphorylcholine	76-93	plasminogen	Mus musculus	149-152
9116283-11	1997	Circulating plasminogen levels were significantly higher in the mice injected with rhIL-6 compared to mice injected with saline.	Sodium Chloride	121-127	plasminogen	Mus musculus	12-23
9157597-5	1997	Lysis of 3H-proline labeled extracellular matrix in the presence of plasminogen with wild-type, t-PA-/- and PAI-1-/- End cells (20% lysis in 48 h with 3 to 5 x 10(6) cells/ml) was comparable, but it was virtually abolished with u-PA-/- End cells.	3h-proline	9-19	plasminogen	Mus musculus	68-79
2044199-2	1991	wt polypeptide with anti-carcinogenic activity, was coupled to poly(D-lysine) (BBI-SS-PDL) and poly(L-glutamate) (BBI-SS-PLG) with a disulfide-cross-linking agent, N-succinimidyl 3-(2-pyridyldithio)propionate (SPDP).	Polyglutamic Acid	95-112	plasminogen	Mus musculus	121-124
8704243-1	1996	Homozygous plasminogen-deficient (Plg-/-) mice had a significantly reduced thrombolytic capacity toward intravenously injected 125I-fibrin labeled plasma clots prepared from Plg-/- murine plasma (9% +/- 3% lysis after 8 hours; (mean +/- SEM, n = 6), as compared with 82% +/- 8% in wild-type mice; P < .0001).	125i-fibrin	127-138	plasminogen	Mus musculus	34-37
8994318-1	1996	Ovalbumin-loaded poly (D,L-lactide co-glycolide) [OVA-loaded PLG] microparticles, produced by emulsion/solvent evaporation stimulated the production of high serum IgG antibody levels after a single subcutaneous (s.c.) administration in mice and the duration of the immune response paralleled the degradation rate of the carrier.	Polylactic Acid-Polyglycolic Acid Copolymer	17-48	plasminogen	Mus musculus	61-64
2044199-2	1991	wt polypeptide with anti-carcinogenic activity, was coupled to poly(D-lysine) (BBI-SS-PDL) and poly(L-glutamate) (BBI-SS-PLG) with a disulfide-cross-linking agent, N-succinimidyl 3-(2-pyridyldithio)propionate (SPDP).	Disulfides	133-142	plasminogen	Mus musculus	121-124
2044199-2	1991	wt polypeptide with anti-carcinogenic activity, was coupled to poly(D-lysine) (BBI-SS-PDL) and poly(L-glutamate) (BBI-SS-PLG) with a disulfide-cross-linking agent, N-succinimidyl 3-(2-pyridyldithio)propionate (SPDP).	N-succinimidyl 3-(2-pyridyldithio)propionate	164-208	plasminogen	Mus musculus	121-124
2044199-2	1991	wt polypeptide with anti-carcinogenic activity, was coupled to poly(D-lysine) (BBI-SS-PDL) and poly(L-glutamate) (BBI-SS-PLG) with a disulfide-cross-linking agent, N-succinimidyl 3-(2-pyridyldithio)propionate (SPDP).	N-succinimidyl 3-(2-pyridyldithio)propionate	210-214	plasminogen	Mus musculus	121-124
34833950-8	2021	Furthermore, nifuroxazide downregulated IL-6, TNF-alpha, NFk-beta, angiostatin, and Jak2 proteins, and it also reduced tumoral VEGF, as indicated by ELISA and immunohistochemical analysis.	nifuroxazide	13-25	plasminogen	Mus musculus	67-78
2116235-5	1990	We have thus followed the course of the plasminogen activator, which converts plasminogen zymogen to plasmin, in liver of S. mansoni-infected mice treated with praziquantel, as schistosomicidal drug.	Praziquantel	160-172	plasminogen	Mus musculus	40-51
2116235-5	1990	We have thus followed the course of the plasminogen activator, which converts plasminogen zymogen to plasmin, in liver of S. mansoni-infected mice treated with praziquantel, as schistosomicidal drug.	Praziquantel	160-172	plasminogen	Mus musculus	78-89
2081600-4	1990	The calculated Mr of mouse plasminogen is 88,706 excluding carbohydrate.	Carbohydrates	59-71	plasminogen	Mus musculus	27-38
2110809-0	1990	Plasminogen activator activity of normal and retinoic acid-treated post-implantation embryos.	Tretinoin	45-58	plasminogen	Mus musculus	0-11
2575971-2	1989	In the mice pretreated with PLG, although the striatal DA level was also reduced, mean DA and 5-HT levels were significantly higher than in mice given MPTP alone.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	151-155	plasminogen	Mus musculus	28-31
34423816-0	2021	Essential role of DNA-PKcs and plasminogen for the development of doxorubicin-induced glomerular injury in mice.	Doxorubicin	66-77	plasminogen	Mus musculus	31-42
35286851-5	2022	Intravenously delivered Ag-conjugated poly(lactide-co-glycolide) NPs (PLG-Ag) distributed largely to the liver, where they associated with both KCs and LSECs.	Polyglactin 910	38-64	plasminogen	Mus musculus	70-73
35286851-7	2022	Ex vivo co-cultures of PLG-Ag-treated KCs or LSECs with Ag-specific CD4 T cells resulted in PGE2 and IL-10 or PGE2 secretion, respectively.	Dinoprostone	92-96	plasminogen	Mus musculus	23-26
35286851-7	2022	Ex vivo co-cultures of PLG-Ag-treated KCs or LSECs with Ag-specific CD4 T cells resulted in PGE2 and IL-10 or PGE2 secretion, respectively.	Dinoprostone	110-114	plasminogen	Mus musculus	23-26
35038117-6	2022	Using mutant PrP (H95A, H110A), we also investigated whether histidine residues outside the octarepeat region in PrP, which is known to bind tPA and Plg, are also involved in their binding.	Histidine	61-70	plasminogen	Mus musculus	149-152
35038117-9	2022	The mutant form of PrP did not stimulate Plg activation to the same degree as apo-PrP indicating that the histidine residues outside the octarepeat region are also involved in binding to tPA and Plg.	Histidine	106-115	plasminogen	Mus musculus	195-198
35038117-11	2022	Our data suggest that upon loss of copper specifically, a structural rearrangement of PrP occurs that exposes binding sites to Plg and tPA, enhancing the stimulation of Plg activation.	Copper	35-41	plasminogen	Mus musculus	127-130
35038117-11	2022	Our data suggest that upon loss of copper specifically, a structural rearrangement of PrP occurs that exposes binding sites to Plg and tPA, enhancing the stimulation of Plg activation.	Copper	35-41	plasminogen	Mus musculus	169-172
35371322-0	2022	Tranexamic acid reduces endometrial cancer effects through the production of angiostatin.	Tranexamic Acid	0-15	plasminogen	Mus musculus	77-88
35371322-9	2022	Furthermore, the macrophage counts and the levels of matrix metalloproteinase (MMP)-12 and angiostatin in tumor cells in the uterus increased compared to the corresponding values in the control group and further increased upon TA treatment.	Tranexamic Acid	227-229	plasminogen	Mus musculus	91-102
35371322-10	2022	The results of our study indicate that TA ameliorated the endometrial cancer induced by MNU and estradiol by regulating the macrophage/MMP-12/plasminogen/angiostatin signal transmission pathway.	Tranexamic Acid	39-41	plasminogen	Mus musculus	154-165
35371322-10	2022	The results of our study indicate that TA ameliorated the endometrial cancer induced by MNU and estradiol by regulating the macrophage/MMP-12/plasminogen/angiostatin signal transmission pathway.	Methylnitrosourea	88-91	plasminogen	Mus musculus	154-165
35371322-10	2022	The results of our study indicate that TA ameliorated the endometrial cancer induced by MNU and estradiol by regulating the macrophage/MMP-12/plasminogen/angiostatin signal transmission pathway.	Estradiol	96-105	plasminogen	Mus musculus	154-165
2575971-3	1989	It is concluded that PLG can prevent, at least partially, the neurotoxic effect of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	83-87	plasminogen	Mus musculus	21-24
2575971-4	1989	We assume that the mechanism of action of PLG may directly or indirectly reduce MPTP-induced dopaminergic neurotoxicity in the nigrostriatal system or reduce the affinity of MPP+ to melanin in DA cells.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	80-84	plasminogen	Mus musculus	42-45
2575971-4	1989	We assume that the mechanism of action of PLG may directly or indirectly reduce MPTP-induced dopaminergic neurotoxicity in the nigrostriatal system or reduce the affinity of MPP+ to melanin in DA cells.	mangion-purified polysaccharide (Candida albicans)	174-178	plasminogen	Mus musculus	42-45
2575971-4	1989	We assume that the mechanism of action of PLG may directly or indirectly reduce MPTP-induced dopaminergic neurotoxicity in the nigrostriatal system or reduce the affinity of MPP+ to melanin in DA cells.	Melanins	182-189	plasminogen	Mus musculus	42-45
4089195-2	1985	Intraperitoneal administrations of prolyl-leucyl-glycinamide (PLG 0.01-10 mg/kg) leads to a dose-dependent inhibition of defeat-induced feeding that is analogous to that obtained after treatment with either the endogenous peptide FMRFamide (Phe-Met-Arg-Phe-NH2), or the prototypic opiate antagonist, naloxone.	Naloxone	300-308	plasminogen	Mus musculus	62-65
2884803-6	1987	In contrast, both PLG and Z-Pro-D-Leu inhibited the development of tolerance to the hypothermic effect of ethanol.	Ethanol	106-113	plasminogen	Mus musculus	18-21
2437428-0	1987	Partial protection from the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by Pro-Leu-Gly-NH2(PLG; MIF-1).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	52-96	plasminogen	Mus musculus	123-126
2437428-0	1987	Partial protection from the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by Pro-Leu-Gly-NH2(PLG; MIF-1).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	98-102	plasminogen	Mus musculus	123-126
2437428-3	1987	In the mice pretreated with PLG, although the striatal dopamine level was also reduced, mean dopamine and serotonin levels were significantly higher than in mice given MPTP alone.	Dopamine	55-63	plasminogen	Mus musculus	28-31
2437428-3	1987	In the mice pretreated with PLG, although the striatal dopamine level was also reduced, mean dopamine and serotonin levels were significantly higher than in mice given MPTP alone.	Dopamine	93-101	plasminogen	Mus musculus	28-31
2437428-3	1987	In the mice pretreated with PLG, although the striatal dopamine level was also reduced, mean dopamine and serotonin levels were significantly higher than in mice given MPTP alone.	Serotonin	106-115	plasminogen	Mus musculus	28-31
2437428-3	1987	In the mice pretreated with PLG, although the striatal dopamine level was also reduced, mean dopamine and serotonin levels were significantly higher than in mice given MPTP alone.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	168-172	plasminogen	Mus musculus	28-31
2437428-4	1987	It is concluded that PLG could protect at least partially the neurotoxic effect of MPTP.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	83-87	plasminogen	Mus musculus	21-24
80946-9	1978	While the Plg-independent proteolytic activity in the supernatants was abolished by EDTA, known to inhibit the neutral proteinases, the Plg-dependent hydrolysis was inhibited by p-nitrophenylguanidinobenzoate, an inhibitor of Plg activator and plasmin.	Edetic Acid	84-88	plasminogen	Mus musculus	10-13
80946-9	1978	While the Plg-independent proteolytic activity in the supernatants was abolished by EDTA, known to inhibit the neutral proteinases, the Plg-dependent hydrolysis was inhibited by p-nitrophenylguanidinobenzoate, an inhibitor of Plg activator and plasmin.	p-nitrophenylguanidinobenzoate	178-208	plasminogen	Mus musculus	10-13
80946-9	1978	While the Plg-independent proteolytic activity in the supernatants was abolished by EDTA, known to inhibit the neutral proteinases, the Plg-dependent hydrolysis was inhibited by p-nitrophenylguanidinobenzoate, an inhibitor of Plg activator and plasmin.	p-nitrophenylguanidinobenzoate	178-208	plasminogen	Mus musculus	136-139
80946-9	1978	While the Plg-independent proteolytic activity in the supernatants was abolished by EDTA, known to inhibit the neutral proteinases, the Plg-dependent hydrolysis was inhibited by p-nitrophenylguanidinobenzoate, an inhibitor of Plg activator and plasmin.	p-nitrophenylguanidinobenzoate	178-208	plasminogen	Mus musculus	136-139
80946-10	1978	These results suggested that the Plg activator secreted by the macrophages generated plasmin, which selectively degraded BP.	Benzo(a)pyrene	121-123	plasminogen	Mus musculus	33-36
80946-11	1978	This interpretation was confirmed by the observation that urokinase, a Plg activator, plus Plg was effective in degrading BP in myelin.	Benzo(a)pyrene	122-124	plasminogen	Mus musculus	71-74
80946-11	1978	This interpretation was confirmed by the observation that urokinase, a Plg activator, plus Plg was effective in degrading BP in myelin.	Benzo(a)pyrene	122-124	plasminogen	Mus musculus	91-94
80946-12	1978	We propose that the action of neutral proteinases released by stimulated macrophages, and its amplification by the Plg-plasmin system, may play a significant role in several inflammatory demyelinating diseases; and that the relative specificity of these reactions for myelin lies in the extreme susceptibility of BP to proteolysis.	Benzo(a)pyrene	313-315	plasminogen	Mus musculus	115-118
33910373-7	2021	In addition, inhibition of lymphangiogenesis by MAZ51, a specific VEGFR3 (vascular endothelial cell growth factor receptor 3) inhibitor, resulted in enhanced inflammatory cell infiltration, gene expression of TNF (tumor necrosis factor)-alpha, IL (interleukin)-1beta, IL-6, TGF (transforming growth factor)-beta, angiostatin, vasohibin, and endostatin, and tissue edema, resulting in reduced angiogenesis.	MAZ51	48-53	plasminogen	Mus musculus	313-324
33388426-12	2021	The enhanced production of angiostatin was attributed to the regulation of the plasminogen proteolysis system via SMI-induced PAI-1 inhibition.	SMI496	114-117	plasminogen	Mus musculus	27-38
32843584-4	2020	RESULTS: DMexo and miR-144-3p mimic-treated MSCs had elevated miR-144-3p levels and decreased MMP9, Ets1 and PLG expression.	dmexo	9-14	plasminogen	Mus musculus	109-112
33492784-1	2021	OBJECTIVE: Plasminogen/plasmin is a serine protease system primarily responsible for degrading fibrin within blood clots.	Serine	36-42	plasminogen	Mus musculus	11-30
32455507-7	2021	RESULTS: Uninduced nphs2Deltaipod *plg-/- mice had normal kidney function and sodium handling.	Sodium	78-84	plasminogen	Mus musculus	35-38
32843584-4	2020	RESULTS: DMexo and miR-144-3p mimic-treated MSCs had elevated miR-144-3p levels and decreased MMP9, Ets1 and PLG expression.	mir-144-3p	19-29	plasminogen	Mus musculus	109-112
31006168-1	2019	AIM: In nephrotic syndrome, aberrantly filtered plasminogen (plg) is converted to active plasmin by tubular urokinase-type plasminogen activator (uPA) and thought to lead to sodium retention by proteolytic activation of the epithelial sodium channel (ENaC).	Sodium	174-180	plasminogen	Mus musculus	61-64
31604031-6	2020	This pathoadaptive response can be mitigated with the PLG inhibitor tranexamic acid (TXA) in a fashion that prevented clinically significant complications in validated murine models of both E. faecalis- and P. aeruginosa mediated colonic perforation.	Tranexamic Acid	68-83	plasminogen	Mus musculus	54-57
31604031-6	2020	This pathoadaptive response can be mitigated with the PLG inhibitor tranexamic acid (TXA) in a fashion that prevented clinically significant complications in validated murine models of both E. faecalis- and P. aeruginosa mediated colonic perforation.	Tranexamic Acid	85-88	plasminogen	Mus musculus	54-57
31006168-3	2019	METHODS: Activation of amiloride-sensitive currents by uPA and plg were studied in Xenopus laevis oocytes expressing murine ENaC.	Amiloride	23-32	plasminogen	Mus musculus	63-66
31006168-5	2019	RESULTS: Experiments in Xenopus laevis oocytes expressing murine ENaC confirmed proteolytic ENaC activation by a combination of plg and uPA which stimulated amiloride-sensitive currents with concomitant cleavage of the ENaC gamma-subunit at the cell surface.	Amiloride	157-166	plasminogen	Mus musculus	128-131
29427239-0	2018	Carbon Dioxide-Generating PLG Nanoparticles for Controlled Anti-Cancer Drug Delivery.	Carbon Dioxide	0-14	plasminogen	Mus musculus	26-29
31851007-1	2021	OBJECTIVE: To investigate the role of bacterial- mediated plasminogen (PLG) activation in the pathogenesis of anastomotic leak (AL) and its mitigation by tranexamic acid (TXA).	Tranexamic Acid	154-169	plasminogen	Mus musculus	71-74
31851007-9	2021	TXA inhibited PLG activation and downstream collagenolysis by pathogens known to have a causal role in AL.	Tranexamic Acid	0-3	plasminogen	Mus musculus	14-17
31851007-10	2021	TXA enema reduced collagenolytic bacteria counts and PLG deposition at anastomotic sites.	Tranexamic Acid	0-3	plasminogen	Mus musculus	53-56
31851007-11	2021	Postoperative PLG inhibition with TXA enema prevented clinically and pathologically apparent pathogen-mediated AL in mice.	Tranexamic Acid	34-37	plasminogen	Mus musculus	14-17
30341568-11	2018	In high-glucose environments, Plg-enhanced VEGF expression and wound healing were suppressed due at least in part to downregulation of keratinocyte-expressed TM.	Glucose	8-15	plasminogen	Mus musculus	30-33
30070662-2	2018	Here, we report the design of a metastable, cancer-targeting siRNA delivery system based on two functional polymers, PVBLG-8, a cationic, helical cell-penetrating polypeptide, and poly(l-glutamic acid) (PLG), an anionic random-coiled polypeptide.	Polymers	107-115	plasminogen	Mus musculus	203-206
29555911-0	2018	Ixonnexin from Tick Saliva Promotes Fibrinolysis by Interacting with Plasminogen and Tissue-Type Plasminogen Activator, and Prevents Arterial Thrombosis.	ixonnexin	0-9	plasminogen	Mus musculus	69-80
29555911-9	2018	Additionally, lysine analogue epsilon-aminocaproic acid inhibits Ixonnexin-mediated plasmin generation implying that lysine-binding sites of Kringle domain(s) of plasminogen or t-PA are involved in this process.	Lysine	14-20	plasminogen	Mus musculus	162-173
29555911-9	2018	Additionally, lysine analogue epsilon-aminocaproic acid inhibits Ixonnexin-mediated plasmin generation implying that lysine-binding sites of Kringle domain(s) of plasminogen or t-PA are involved in this process.	Aminocaproic Acid	30-55	plasminogen	Mus musculus	162-173
29555911-9	2018	Additionally, lysine analogue epsilon-aminocaproic acid inhibits Ixonnexin-mediated plasmin generation implying that lysine-binding sites of Kringle domain(s) of plasminogen or t-PA are involved in this process.	ixonnexin	65-74	plasminogen	Mus musculus	162-173
29555911-9	2018	Additionally, lysine analogue epsilon-aminocaproic acid inhibits Ixonnexin-mediated plasmin generation implying that lysine-binding sites of Kringle domain(s) of plasminogen or t-PA are involved in this process.	Lysine	117-123	plasminogen	Mus musculus	162-173
29555911-10	2018	Moreover, surface plasmon resonance experiments shows that Ixonnexin binds t-PA, and plasminogen (KD 10 nM), but not urokinase.	ixonnexin	59-68	plasminogen	Mus musculus	85-96
29555911-11	2018	These results imply that Ixonnexin promotes fibrinolysis by supporting the interaction of plasminogen with t-PA through formation of an enzymatically productive ternary complex.	ixonnexin	25-34	plasminogen	Mus musculus	90-101
31462325-4	2019	METHODS: Mice were treated with an antisense oligonucleotide to deplete liver-produced PLG prior to systemic challenge with lipopolysaccharide (LPS), a major component of the outer membrane of gram-negative bacteria, known to induce a strong immune response in animals.	Oligonucleotides	45-60	plasminogen	Mus musculus	87-90
31462325-8	2019	CONCLUSIONS: Depletion of plasma PLG with an antisense oligonucleotide dramatically reduced glial cell activation and perivascular macrophage migration into the brain following LPS injection.	Oligonucleotides	55-70	plasminogen	Mus musculus	33-36
29427239-1	2018	PURPOSE: Poly(D,L-lactide-co-glycolide) (PLG) nanoparticles containing doxorubicin and mineralized calcium carbonate were fabricated and their anti-tumor efficacy was tested using a neuroblastoma-bearing mouse model.	Polylactic Acid-Polyglycolic Acid Copolymer	9-39	plasminogen	Mus musculus	41-44
29427239-1	2018	PURPOSE: Poly(D,L-lactide-co-glycolide) (PLG) nanoparticles containing doxorubicin and mineralized calcium carbonate were fabricated and their anti-tumor efficacy was tested using a neuroblastoma-bearing mouse model.	Doxorubicin	71-82	plasminogen	Mus musculus	41-44
29427239-1	2018	PURPOSE: Poly(D,L-lactide-co-glycolide) (PLG) nanoparticles containing doxorubicin and mineralized calcium carbonate were fabricated and their anti-tumor efficacy was tested using a neuroblastoma-bearing mouse model.	Calcium Carbonate	99-116	plasminogen	Mus musculus	41-44
29427239-2	2018	METHODS: PLG nanoparticles were prepared by a double emulsion (water-in-oil-in-water; W/O/W) method.	Water	63-68	plasminogen	Mus musculus	9-12
29427239-2	2018	METHODS: PLG nanoparticles were prepared by a double emulsion (water-in-oil-in-water; W/O/W) method.	Oils	72-75	plasminogen	Mus musculus	9-12
29427239-2	2018	METHODS: PLG nanoparticles were prepared by a double emulsion (water-in-oil-in-water; W/O/W) method.	Water	79-84	plasminogen	Mus musculus	9-12
29427239-3	2018	Calcium carbonate was mineralized within the PLG nanoparticles during the emulsion process.	Calcium Carbonate	0-17	plasminogen	Mus musculus	45-48
29427239-7	2018	RESULTS: Mineralized calcium carbonate in PLG nanoparticles was ionized at acidic pH and generated carbon dioxide gas, which resultantly accelerated the release of doxorubicin from the nanoparticles.	Calcium Carbonate	21-38	plasminogen	Mus musculus	42-45
29427239-7	2018	RESULTS: Mineralized calcium carbonate in PLG nanoparticles was ionized at acidic pH and generated carbon dioxide gas, which resultantly accelerated the release of doxorubicin from the nanoparticles.	Carbon Dioxide	99-113	plasminogen	Mus musculus	42-45
29427239-7	2018	RESULTS: Mineralized calcium carbonate in PLG nanoparticles was ionized at acidic pH and generated carbon dioxide gas, which resultantly accelerated the release of doxorubicin from the nanoparticles.	Doxorubicin	164-175	plasminogen	Mus musculus	42-45
29427239-8	2018	RVG peptide-modified, gas-generating PLG nanoparticles showed a significantly enhanced targeting ability to neuroblastoma and an increased therapeutic efficacy in vivo as compared with free doxorubicin.	Doxorubicin	190-201	plasminogen	Mus musculus	37-40
29423262-2	2018	Herein, polymeric micelles incorporated with cisplatin are prepared based on the complexation between CDDP and hydrophilic poly (L-glutamic acid)-b-poly (2-methacryloyloxyethyl phosphorylcholine) (PLG-b-PMPC) diblock copolymers.	Cisplatin	45-54	plasminogen	Mus musculus	197-200
29423262-2	2018	Herein, polymeric micelles incorporated with cisplatin are prepared based on the complexation between CDDP and hydrophilic poly (L-glutamic acid)-b-poly (2-methacryloyloxyethyl phosphorylcholine) (PLG-b-PMPC) diblock copolymers.	Cisplatin	102-106	plasminogen	Mus musculus	197-200
29423262-2	2018	Herein, polymeric micelles incorporated with cisplatin are prepared based on the complexation between CDDP and hydrophilic poly (L-glutamic acid)-b-poly (2-methacryloyloxyethyl phosphorylcholine) (PLG-b-PMPC) diblock copolymers.	poly (l-glutamic acid)-b-poly (2-methacryloyloxyethyl phosphorylcholine)	123-195	plasminogen	Mus musculus	197-200
29423262-7	2018	Thus, PLG-b-PMPC copolymer might be a promising carrier for CDDP incorporating in cancer therapy.	copolymer	17-26	plasminogen	Mus musculus	6-9
29423262-7	2018	Thus, PLG-b-PMPC copolymer might be a promising carrier for CDDP incorporating in cancer therapy.	Cisplatin	60-64	plasminogen	Mus musculus	6-9
28345891-5	2017	The synthesized star shaped poly(d,l-lactide)-b-gelatin (ss-pLG) exhibited enhanced wettability and protein adsorption.	poly(lactide)	28-44	plasminogen	Mus musculus	60-63
28768900-0	2017	Plasminogen promotes cholesterol efflux by the ABCA1 pathway.	Cholesterol	21-32	plasminogen	Mus musculus	0-11
28345891-11	2017	In addition to that, burst release of docetaxal (DTX) was observed from ss-pLG scaffolds.	Docetaxal	38-47	plasminogen	Mus musculus	75-78
28345891-11	2017	In addition to that, burst release of docetaxal (DTX) was observed from ss-pLG scaffolds.	Digitoxigenin	49-52	plasminogen	Mus musculus	75-78
27592166-3	2016	Plg may regulate the DPP-4 activity and the glucose metabolism.	Glucose	44-51	plasminogen	Mus musculus	0-3
27090890-11	2016	Further comparison of the immune responses to the proteins adjuvanted with PLG or Montanide  ISA 206 VG 6 weeks after the last immunization revealed that antigens encapsulated in PLG conferred greater protective immunity against challenge.	montanide	82-91	plasminogen	Mus musculus	179-182
27091976-6	2016	Antigen-conjugated NPs made of biodegradable poly(lactide-co-glycolide) (Ag-PLG) are similarly effective prophylactically, are well tolerated by sensitized animals, but only partially inhibit Th2 responses when administered therapeutically.	Polyglactin 910	45-71	plasminogen	Mus musculus	76-79
27091976-6	2016	Antigen-conjugated NPs made of biodegradable poly(lactide-co-glycolide) (Ag-PLG) are similarly effective prophylactically, are well tolerated by sensitized animals, but only partially inhibit Th2 responses when administered therapeutically.	th2	192-195	plasminogen	Mus musculus	76-79
26573885-3	2016	Thus, biocompatible poly(d,l-lactide-co-glycolide) (PLG) nanoparticles containing an imaging probe and therapeutic gene are prepared, followed by modification with rabies virus glycoprotein (RVG) peptide for neuroblastoma-targeting delivery.	Polylactic Acid-Polyglycolic Acid Copolymer	20-50	plasminogen	Mus musculus	52-55
20163454-3	2010	Treatment with the broad spectrum MMP inhibitor, galardin, delays wound healing in wildtype mice and completely arrest wound healing in plasminogen (Plg)-deficient mice, indicating a functional overlap between plasmin- and galardin-sensitive MMPs during wound healing.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	49-57	plasminogen	Mus musculus	136-147
24732409-11	2014	BDA-positive axonal density of the CST originating from the contralesional cortex in the denervated side of the cervical gray matter was significantly reduced in Plg-/- mice compared with Plg+/+ mice (p<0.05).	biotinylated dextran amine	0-3	plasminogen	Mus musculus	162-165
24732409-11	2014	BDA-positive axonal density of the CST originating from the contralesional cortex in the denervated side of the cervical gray matter was significantly reduced in Plg-/- mice compared with Plg+/+ mice (p<0.05).	biotinylated dextran amine	0-3	plasminogen	Mus musculus	188-191
24297047-5	2014	Angiostatin conjugated to FITC revealed that angiostatin was endocytozed by activated mouse and human neutrophils in a lipid raft-dependent fashion.	Fluorescein-5-isothiocyanate	26-30	plasminogen	Mus musculus	0-11
24297047-5	2014	Angiostatin conjugated to FITC revealed that angiostatin was endocytozed by activated mouse and human neutrophils in a lipid raft-dependent fashion.	Fluorescein-5-isothiocyanate	26-30	plasminogen	Mus musculus	45-56
24297047-8	2014	Angiostatin treatment, before or after LPS-induced neutrophil activation, inhibited phosphorylation of p38 and p44/42 MAPKs, abolished reactive oxygen species production and released the neutrophils from suppressed apoptosis, as indicated by expression of activated caspase-3 and morphological evidence of apoptosis.	Reactive Oxygen Species	135-158	plasminogen	Mus musculus	0-11
22393105-0	2013	Effect of angiostatin on 1,2-dimethylhydrazine-induced colon cancer in mice.	1,2-Dimethylhydrazine	25-46	plasminogen	Mus musculus	10-21
23811964-6	2013	H2S therapy increased the expression of the proangiogenic factor, vascular endothelial cell growth factor, and decreased the angiogenesis inhibitor, angiostatin.	Hydrogen Sulfide	0-3	plasminogen	Mus musculus	149-160
22393105-13	2013	The administration period of angiostatin corresponds to the precancerous period and the reduction in the number of lesions could be important for the protective function of angiostatin in DMH + angiostain group.	1,2-Dimethylhydrazine	188-191	plasminogen	Mus musculus	29-40
22393105-13	2013	The administration period of angiostatin corresponds to the precancerous period and the reduction in the number of lesions could be important for the protective function of angiostatin in DMH + angiostain group.	1,2-Dimethylhydrazine	188-191	plasminogen	Mus musculus	173-184
24762227-3	2013	In this study, we have examined the antitumoral function of the IL-12 gene cotransfected with antiangiogenic genes for angiostatin K1-3, endostatin, and saxatilin by O,O"-dimyristyl-N-lysyl glutamate (DMKE) cationic liposomes in a mouse tumor model.	O,O'-dimyristyl-N-lysyl glutamate	166-199	plasminogen	Mus musculus	119-130
22056679-8	2012	The observed sex-linked erythropoietic defect was attributed to decreased serum testosterone levels in Plg KO mice as a consequence of impaired secretion of the pituitary luteinizing hormone (LH) under steady-state condition.	Testosterone	80-92	plasminogen	Mus musculus	103-106
22419888-2	2012	We previously reported that H2S inhibits antiangiogenic factors such, as endostatin and angiostatin, but a little is known about its effect on parstatin (a fragment of proteinase-activated receptor-1, PAR-1).	Hydrogen Sulfide	28-31	plasminogen	Mus musculus	88-99
21915104-0	2012	Bevacizumab with angiostatin-armed oHSV increases antiangiogenesis and decreases bevacizumab-induced invasion in U87 glioma.	ohsv	35-39	plasminogen	Mus musculus	17-28
21233344-6	2011	In the NaHS-treated AB 8 wk group, the expression of MMP-2, CD31, and VEGF was increased while the expression of MMP-9, endostatin, angiostatin, and tissue inhibitor of matrix metalloproteinase (TIMP)-3 was decreased compared with untreated control mice.	sodium bisulfide	7-11	plasminogen	Mus musculus	132-143
21755014-9	2011	Binding of the recombinant proteins to PLG or ECM components was assessed by using antibodies against each of the recombinant proteins obtained in mice and confirmed by monoclonal anti-polyhistidine antibodies.	polyhistidine	185-198	plasminogen	Mus musculus	39-42
20163454-3	2010	Treatment with the broad spectrum MMP inhibitor, galardin, delays wound healing in wildtype mice and completely arrest wound healing in plasminogen (Plg)-deficient mice, indicating a functional overlap between plasmin- and galardin-sensitive MMPs during wound healing.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	49-57	plasminogen	Mus musculus	149-152
18562486-6	2008	polyI was unable to trigger IFN-alpha production, and it was efficiently inducing Plg and TF.	Poly I	0-5	plasminogen	Mus musculus	82-85
19465692-4	2009	After internalization of angiostatin into the cell, at least 2 proteins within the mitochondria bind this molecule: malate dehydrogenase, a member of Krebs cycle, and adenosine triphosphate synthase.	krebs	150-155	plasminogen	Mus musculus	25-36
18677407-6	2008	After induction of peritonitis by thioglycollate injection, we found that Plg(-/-) mice displayed diminished macrophage trans-ECM migration and decreased MMP-9 activation.	Thioglycolates	34-48	plasminogen	Mus musculus	74-77
18677407-8	2008	We used periaortic application of CaCl2 to induce abdominal aortic aneurysm (AAA) and found that Plg(-/-) mice displayed reduced macrophage infiltration and were protected from aneurysm formation.	Calcium Chloride	34-39	plasminogen	Mus musculus	97-100
21614211-0	2010	Mouse plasminogen has oxidized phosphatidylcholine adducts that are not metabolized by lipoprotein-associated phospholipase A2under basal conditions.	Phosphatidylcholines	31-50	plasminogen	Mus musculus	6-17
18562486-9	2008	Importantly, the presence of U- and C-nucleotide strands in the dsRNA significantly reduced expression of Plg and TF compared with polyI alone.	u- and c-nucleotide	29-48	plasminogen	Mus musculus	106-109
18562486-9	2008	Importantly, the presence of U- and C-nucleotide strands in the dsRNA significantly reduced expression of Plg and TF compared with polyI alone.	Poly I	131-136	plasminogen	Mus musculus	106-109
17320947-6	2007	Eighty percent of the FGF-2 was released at controlled rates from gelatin-polylysine (gelatin-PLL) and gelatin-polyglutamic acid (gelatin-PLG) hydrogel scaffolds over a period of 28 days.	Polyglutamic Acid	111-128	plasminogen	Mus musculus	138-141
18311818-10	2008	Treatment of Plg(-/-) mice with antibiotic (cloxacillin) resulted in successful killing of the bacteria, but the necrotic tissue remained in the infected joints.	Cloxacillin	44-55	plasminogen	Mus musculus	13-16
17683059-1	2008	The objective of this work was to evaluate the potency of the CpG containing oligonucleotide encapsulated within poly(lactide-co-glycolide), and coadministered with antigen adsorbed to poly(lactide-co-glycolide) microparticles (PLG particles).	Oligonucleotides	77-92	plasminogen	Mus musculus	228-231
17690254-5	2007	All 4 Plg-Rs were present on the surface of these cells and showed enhanced expression on the thioglycollate-induced macrophages compared with peripheral blood monocytes.	Thioglycolates	94-108	plasminogen	Mus musculus	6-9
17541016-6	2007	Bronchoalveolar lavage demonstrated a marked increase in eosinophils and lymphocytes in ovalbumin-treated Plg(+/+) mice, which were reduced to phosphate-buffered saline-treated control levels in Plg(+/-) or Plg(-/-) mice.	Phosphate-Buffered Saline	143-168	plasminogen	Mus musculus	195-198
17541016-6	2007	Bronchoalveolar lavage demonstrated a marked increase in eosinophils and lymphocytes in ovalbumin-treated Plg(+/+) mice, which were reduced to phosphate-buffered saline-treated control levels in Plg(+/-) or Plg(-/-) mice.	Phosphate-Buffered Saline	143-168	plasminogen	Mus musculus	195-198
17541016-9	2007	Administration of the plasminogen inhibitor, tranexamic acid, reduced eosinophil and lymphocyte numbers, mucus production, and collagen deposition in the lungs of ovalbumin-treated Plg(+/+) mice.	Tranexamic Acid	45-60	plasminogen	Mus musculus	22-33
17541016-9	2007	Administration of the plasminogen inhibitor, tranexamic acid, reduced eosinophil and lymphocyte numbers, mucus production, and collagen deposition in the lungs of ovalbumin-treated Plg(+/+) mice.	Tranexamic Acid	45-60	plasminogen	Mus musculus	181-184
16840775-5	2006	A recent study using bleomycin-exposed mice showed that manipulations of the plasminogen activation system influenced the amount of free HGF within bronchoalveolar lavage fluid without affecting total lung HGF mRNA or protein.	Bleomycin	21-30	plasminogen	Mus musculus	77-88
17122079-4	2007	We found that CL formed normally not only in plasminogen-deficient mice and in galardin-treated wild-type mice, but also in galardin-treated plg-deficient mice, suggesting that neither of the plasminogen activator and MMP systems is essential for CL formation.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	124-132	plasminogen	Mus musculus	141-144
17122079-5	2007	Nevertheless, in plg-deficient mice, serum progesterone levels were reduced by approximately 50%, and the progesterone levels were not reduced further by galardin treatment.	Progesterone	43-55	plasminogen	Mus musculus	17-20
17293777-8	2007	RESULTS: The rAAV-angiostatin injections led to sustained angiostatin gene expression in retina as confirmed by RT-PCR, and reduced extravascular albumin accumulation in STZ-induced diabetic retina.	Streptozocin	170-173	plasminogen	Mus musculus	18-29
17293777-11	2007	rAAV-angiostatin reduced retinal occludin loss at 10 days after STZ-induced diabetes (n=5, p=0.041).	Streptozocin	64-67	plasminogen	Mus musculus	5-16
17293777-13	2007	CONCLUSIONS: Intravitreal delivery of rAAV-angiostatin reduces vascular leakage in an STZ-induced diabetic model.	Streptozocin	86-89	plasminogen	Mus musculus	43-54
16952557-1	2006	BACKGROUND & AIMS: The plasminogen (plg) system participates in tissue repair in several organs, but its role in pancreas repair remains poorly characterized.	Adenosine Monophosphate	12-15	plasminogen	Mus musculus	27-38
16949567-1	2006	The extracellular serine protease, plasmin, is activated from its precursor, plasminogen (Plg), by the urokinase-type and tissue-type Plg activators (uPA and tPA respectively).	Tetradecanoylphorbol Acetate	158-161	plasminogen	Mus musculus	77-88
16949567-1	2006	The extracellular serine protease, plasmin, is activated from its precursor, plasminogen (Plg), by the urokinase-type and tissue-type Plg activators (uPA and tPA respectively).	Tetradecanoylphorbol Acetate	158-161	plasminogen	Mus musculus	90-93
16643891-3	2006	We earlier reported that angiostatin binds to cell surface annexin II through the lysine-binding domain (kringles 1-4) [Tuszynski, G.P., Sharma, M., Rothman, V.L., Sharma, M.C., 2002.	Lysine	82-88	plasminogen	Mus musculus	25-36
16643891-4	2006	Angiostatin binds to tyrosine kinase substrate annexin II through the lysine-binding domain in endothelial cells.	Lysine	70-76	plasminogen	Mus musculus	0-11
16643891-11	2006	Angiostatin also reduced plasmin generation by 81.6%, suggesting that angiostatin may be competing with plasminogen through lysine-binding domain.	Lysine	124-130	plasminogen	Mus musculus	0-11
16643891-11	2006	Angiostatin also reduced plasmin generation by 81.6%, suggesting that angiostatin may be competing with plasminogen through lysine-binding domain.	Lysine	124-130	plasminogen	Mus musculus	70-81
16952557-1	2006	BACKGROUND & AIMS: The plasminogen (plg) system participates in tissue repair in several organs, but its role in pancreas repair remains poorly characterized.	Adenosine Monophosphate	12-15	plasminogen	Mus musculus	40-43
16753063-4	2006	In previous studies, it has been demonstrated that administration of PA in combination with the free sulfhydryl donor (FSD) agents captopril or N-acetyl cysteine, resulted in angiostatin generation, and anti-angiogenic and anti-tumour activity in murine models.	Captopril	131-140	plasminogen	Mus musculus	175-186
16763560-3	2006	Skin wounds in uPA;tPA-deficient mice treated with the broad-spectrum matrix metalloproteinase (MMP) inhibitor galardin (N-[(2R)-2-(hydroxamido-carbonylmethyl)-4-methylpentanoyl]-L-tryptophan methylamide) eventually heal, whereas skin wounds in galardin-treated Plg-deficient mice do not heal.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	111-119	plasminogen	Mus musculus	262-265
16763560-5	2006	In vivo administration of a plasma kallikrein (pKal)-selective form of the serine protease inhibitor ecotin exacerbates the healing impairment of uPA;tPA double-deficient wounds to a degree indistinguishable from that observed in Plg-deficient mice, and completely blocks the activity of pKal, but not uPA and tPA in wound extracts.	ecotin	101-107	plasminogen	Mus musculus	230-233
16712832-4	2006	We found that in both wild-type mice and heterozygous plg-deficient (plg+/-) mice that had been treated with galardin prior to ovulation, there was a mild (18-20%) reduction in ovulation efficiency.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	109-117	plasminogen	Mus musculus	54-57
16712832-4	2006	We found that in both wild-type mice and heterozygous plg-deficient (plg+/-) mice that had been treated with galardin prior to ovulation, there was a mild (18-20%) reduction in ovulation efficiency.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	109-117	plasminogen	Mus musculus	69-72
16712832-5	2006	Surprisingly, galardin treatment of plg-deficient (plg-/-) mice only caused an additional 14% reduction in ovulation efficiency as compared to vehicle-treated plg-/- mice.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	14-22	plasminogen	Mus musculus	36-39
16712832-5	2006	Surprisingly, galardin treatment of plg-deficient (plg-/-) mice only caused an additional 14% reduction in ovulation efficiency as compared to vehicle-treated plg-/- mice.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	14-22	plasminogen	Mus musculus	51-54
16712832-5	2006	Surprisingly, galardin treatment of plg-deficient (plg-/-) mice only caused an additional 14% reduction in ovulation efficiency as compared to vehicle-treated plg-/- mice.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	14-22	plasminogen	Mus musculus	51-54
16753063-4	2006	In previous studies, it has been demonstrated that administration of PA in combination with the free sulfhydryl donor (FSD) agents captopril or N-acetyl cysteine, resulted in angiostatin generation, and anti-angiogenic and anti-tumour activity in murine models.	Acetylcysteine	144-161	plasminogen	Mus musculus	175-186
16753063-6	2006	D-penicillamine proved to be most efficient in supporting the conversion of plasminogen to angiostatin in vitro.	Penicillamine	0-15	plasminogen	Mus musculus	91-102
16753063-9	2006	RESULTS: Surprisingly, we found that despite the superior angiostatin generating capacity of D-penicillamine in vitro, both in vivo angiostatin generation and anti-tumour effects of tPA/D-penicillamine treatment were impaired compared to our previous studies with tPA and captopril.	Penicillamine	93-108	plasminogen	Mus musculus	58-69
16124051-2	2005	METHODS: The recombinant vector pcDNA3.1(+)-angiostatin was transfected into human pancreatic cancer cells PC-3 with Lipofectamine 2000, and paralleled with the vector and mock control.	Lipofectamine	117-135	plasminogen	Mus musculus	44-55
15205911-1	2005	We examined the feasibility of the human immunodeficiency virus (HIV) vector-mediated local expression of angiostatin in the treatment of murine collagen-induced arthritis in a mouse model generated by immunization with bovine type II collagen and Freund"s complete adjuvant.	freund"s	248-256	plasminogen	Mus musculus	106-117
16611153-4	2006	The central components of the PA system are the proteolytic activators, urokinase-plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA), plasminogen (plg) and its degradation product, plasmin, together with the major inhibitors of this system, plasminogen activator inhibitor-1 and -2 (PAI-1, PAI-2).	Protactinium	30-32	plasminogen	Mus musculus	82-93
16611153-4	2006	The central components of the PA system are the proteolytic activators, urokinase-plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA), plasminogen (plg) and its degradation product, plasmin, together with the major inhibitors of this system, plasminogen activator inhibitor-1 and -2 (PAI-1, PAI-2).	Protactinium	30-32	plasminogen	Mus musculus	170-173
16253809-0	2005	Distribution and pharmacokinetic analysis of angiostatin radioiodine labeled with high stability.	Iodine-131	57-68	plasminogen	Mus musculus	45-56
16253809-3	2005	In this study, we synthesized an AST probe radioiodinated via the Bolton-Hunter reagent (125I-BH-AST) and investigated its stability and biokinetics in mice.	125i-bh	89-96	plasminogen	Mus musculus	33-36
16253809-3	2005	In this study, we synthesized an AST probe radioiodinated via the Bolton-Hunter reagent (125I-BH-AST) and investigated its stability and biokinetics in mice.	125i-bh	89-96	plasminogen	Mus musculus	97-100
16253809-4	2005	METHODS: 125I-BH-AST and conventional direct radioiodinated 125I-AST were evaluated for human endothelial cell binding characteristics.	125i-bh	9-16	plasminogen	Mus musculus	17-20
16253809-6	2005	Angiostatin pharmacokinetics was analyzed by serial blood sampling after intravenous injection of 125I-BH-AST with varying AST concentrations in mice.	125i-bh	98-105	plasminogen	Mus musculus	0-11
16253809-6	2005	Angiostatin pharmacokinetics was analyzed by serial blood sampling after intravenous injection of 125I-BH-AST with varying AST concentrations in mice.	125i-bh	98-105	plasminogen	Mus musculus	106-109
16253809-10	2005	Kinetic analysis of 125I-BH-AST revealed AST to have linear pharmacokinetics with a T(1/2) of 5.8+/-2.6 h, volume of distribution (V(d)) of 6.8+/-1.3 ml and clearance of 0.8+/-0.1 ml/h.	125i-bh	20-27	plasminogen	Mus musculus	28-31
16253809-10	2005	Kinetic analysis of 125I-BH-AST revealed AST to have linear pharmacokinetics with a T(1/2) of 5.8+/-2.6 h, volume of distribution (V(d)) of 6.8+/-1.3 ml and clearance of 0.8+/-0.1 ml/h.	125i-bh	20-27	plasminogen	Mus musculus	41-44
16253809-11	2005	CONCLUSION: Radioiodine-labeled AST prepared by the BH method provides a radioprobe with superior stability and improved in vivo biokinetics that is useful for distribution and pharmacokinetic studies.	Iodine-131	12-23	plasminogen	Mus musculus	32-35
15486558-4	2005	Expression vectors encoding angiostatin and endostatin, formulated with poly-N-vinyl pyrrolidone (PVP), were injected into the tibialis and gastrocnemia muscles, leading to expression of angiostatin and endostatin in muscle fibers.	Povidone	98-101	plasminogen	Mus musculus	187-198
15841177-4	2005	Mice deficient in MMP-9 were resistant to experimental BP, while mice deficient in Plg and both tissue Plg activator (tPA) and urokinase Plg activator (uPA) showed delayed and less intense blister formation induced by antibodies to BP180.	Tetradecanoylphorbol Acetate	118-121	plasminogen	Mus musculus	103-106
15841177-4	2005	Mice deficient in MMP-9 were resistant to experimental BP, while mice deficient in Plg and both tissue Plg activator (tPA) and urokinase Plg activator (uPA) showed delayed and less intense blister formation induced by antibodies to BP180.	Tetradecanoylphorbol Acetate	118-121	plasminogen	Mus musculus	103-106
14716496-6	2004	Angiostatin mice received carbon tetrachloride for 5 weeks and angiostatin during weeks 4 and 5.	Carbon Tetrachloride	26-46	plasminogen	Mus musculus	0-11
15352048-6	2004	First, we determined the optimal conditions for in vitro angiostatin generation by incubating murine plasma with different concentrations of plasminogen activator and/or the FSD captopril.	Captopril	178-187	plasminogen	Mus musculus	57-68
15352048-10	2004	Angiostatin was readily detectable in mice receiving both tPA and captopril, but not in mice receiving either one of the agents.	Captopril	66-75	plasminogen	Mus musculus	0-11
15569437-0	2004	[The inhibitory effects of angiostatin on retinal neovascularization induced by oxygen].	Oxygen	80-86	plasminogen	Mus musculus	27-38
15569437-2	2004	METHODS: Angiostatin was purified with L-lysine Sepharose 4B from human plasma.	l-lysine sepharose 4b	39-60	plasminogen	Mus musculus	9-20
15133846-15	2004	CONCLUSION: Angiostatin cDNA could be stably expressed in human hepatocellular carcinoma cell line SMMC-7721 without obvious inhibitory effects on the growth of SMMC-7721 cells.	smmc	99-103	plasminogen	Mus musculus	12-23
15128731-1	2004	Poly (DL-lactide-co-glycolide) (PLG) nanoparticles encapsulating three front-line antitubercular drugs, i.e. rifampicin, isoniazid and pyrazinamide, were prepared by the multiple emulsion technique and administered subcutaneously to mice for pharmacokinetic/chemotherapeutic study.	poly (dl-lactide-co-glycolide	0-29	plasminogen	Mus musculus	32-35
15128731-1	2004	Poly (DL-lactide-co-glycolide) (PLG) nanoparticles encapsulating three front-line antitubercular drugs, i.e. rifampicin, isoniazid and pyrazinamide, were prepared by the multiple emulsion technique and administered subcutaneously to mice for pharmacokinetic/chemotherapeutic study.	Rifampin	109-119	plasminogen	Mus musculus	32-35
15128731-1	2004	Poly (DL-lactide-co-glycolide) (PLG) nanoparticles encapsulating three front-line antitubercular drugs, i.e. rifampicin, isoniazid and pyrazinamide, were prepared by the multiple emulsion technique and administered subcutaneously to mice for pharmacokinetic/chemotherapeutic study.	Pyrazinamide	135-147	plasminogen	Mus musculus	32-35
15302998-0	2004	Angiogenesis inhibition by angiostatin, endostatin and TNP-470 prevents cyclophosphamide induced cystitis.	Cyclophosphamide	72-88	plasminogen	Mus musculus	27-38
14717962-2	2004	An internal fragment of plasminogen, angiostatin consists of kringle domains that are known to be lysine-binding.	Lysine	98-104	plasminogen	Mus musculus	37-48
14651966-0	2003	Plasminogen-induced IL-1beta and TNF-alpha production in microglia is regulated by reactive oxygen species.	Reactive Oxygen Species	83-106	plasminogen	Mus musculus	0-11
14651966-6	2003	Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells.	Reactive Oxygen Species	0-23	plasminogen	Mus musculus	68-79
14651966-6	2003	Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells.	Reactive Oxygen Species	0-23	plasminogen	Mus musculus	152-163
14651966-6	2003	Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells.	Reactive Oxygen Species	0-23	plasminogen	Mus musculus	152-163
14651966-6	2003	Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells.	Reactive Oxygen Species	25-28	plasminogen	Mus musculus	68-79
14651966-6	2003	Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells.	Reactive Oxygen Species	116-119	plasminogen	Mus musculus	68-79
14651966-6	2003	Reactive oxygen species (ROS) appeared to play an important role in plasminogen-induced microglial activation, with ROS being generated within 15min of plasminogen treatment, and antioxidants (100 microM trolox and 10mM NAC) reducing IL-1beta and TNF-alpha expression in plasminogen-treated cells.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	204-210	plasminogen	Mus musculus	68-79
14651966-7	2003	Furthermore, plasminogen stimulated CREB and NF-kappaB DNA binding activity, and this activation was also reduced by trolox and NAC.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	117-123	plasminogen	Mus musculus	13-24
14651966-8	2003	These results suggest that plasminogen activates microglia via stimulation of ROS production.	Reactive Oxygen Species	78-81	plasminogen	Mus musculus	27-38