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1. Full Text CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer
by Xie, C and Jiang, X.H and Zhang, J.T and Sun, T.T and Dong, J.D and Sanders, A.J and Diao, R.Y and Wang, Y and Fok, K.L and Tsang, L.L and Yu, M.K and Zhang, X.H and Chung, Y.W and Ye, L and Zhao, M.Y and Guo, J.H and Xiao, Z.J and Lan, H.Y and Ng, C.F and Lau, K.M and Cai, Z.M and Jiang, W.G and Chan, H.C
Oncogene, ISSN 0950-9232, 05/2013, Volume 32, Issue 18, pp. 2282 - 2291
Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is expressed in the epithelial cells of a wide range of organs/tissues from which most cancers... 
CFTR | miR-193b | uPA | MUC4 EXPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | PANCREATIC ADENOCARCINOMA | CELL MIGRATION | MESENCHYMAL TRANSITION | MIR-200 FAMILY | CELL BIOLOGY | TRANSMEMBRANE CONDUCTANCE REGULATOR | BREAST-CANCER | HEPATOCELLULAR-CARCINOMA | ONCOLOGY | GENETICS & HEREDITY | NF-KAPPA-B | CYSTIC-FIBROSIS GENE | Prostatic Neoplasms - metabolism | Receptors, Urokinase Plasminogen Activator - immunology | Humans | Gene Expression Regulation, Neoplastic | Molecular Sequence Data | Male | Cell Movement - genetics | Gene Knockdown Techniques | Prostatic Neoplasms - genetics | Base Sequence | Female | Urokinase-Type Plasminogen Activator - immunology | Prostatic Neoplasms - pathology | Down-Regulation | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Urokinase-Type Plasminogen Activator - genetics | Receptors, Urokinase Plasminogen Activator - metabolism | Xenograft Model Antitumor Assays | Animals | Urokinase-Type Plasminogen Activator - metabolism | Mice, Nude | Cell Line, Tumor | Cystic Fibrosis Transmembrane Conductance Regulator - genetics | Mice | MicroRNAs - genetics | Receptors, Urokinase Plasminogen Activator - genetics | Urokinase | Tissue plasminogen activator | Physiological aspects | Development and progression | Tumor suppressor genes | Genetic aspects | Research | Prostate cancer | Cystic fibrosis | Membranes | Tumors
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2. Full Text Plasminogen Activator Inhibitor-1 Reduces Tissue-Type Plasminogen Activator–Dependent Fibrinolysis and Intrahepatic Hemorrhage in Experimental Acetaminophen Overdose
by Pant, Asmita and Kopec, Anna K and Baker, Kevin S and Cline-Fedewa, Holly and Lawrence, Daniel A and Luyendyk, James P
The American Journal of Pathology, ISSN 0002-9440, 05/2018, Volume 188, Issue 5, pp. 1204 - 1212
Acetaminophen (APAP)–induced liver injury in mice is associated with activation of the coagulation cascade and deposition of fibrin in liver. Plasminogen... 
ACUTE LIVER-FAILURE | FIBROSIS | BILE-DUCT LIGATION | REGENERATION | IN-VIVO | INJURY | CONSEQUENCES | PAI-1 | MICE | REBALANCED HEMOSTASIS | PATHOLOGY | Drug Overdose - metabolism | Fibrinolysis - drug effects | Hemorrhage - genetics | Liver Diseases - genetics | Drug Overdose - genetics | Tissue Plasminogen Activator - metabolism | Hemorrhage - complications | Hemorrhage - metabolism | Tissue Plasminogen Activator - genetics | Mice, Knockout | Animals | Plasminogen Activator Inhibitor 1 - metabolism | Acetaminophen - poisoning | Liver Diseases - complications | Drug Overdose - complications | Mice | Plasminogen Activator Inhibitor 1 - genetics | Liver Diseases - metabolism
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3. Full Text Endogenous plasminogen activators mediate progressive intracerebral hemorrhage after traumatic brain injury in mice
by Hijazi, Nuha and Fanne, Rami Abu and Abramovitch, Rinat and Yarovoi, Serge and Higazi, Muhamed and Abdeen, Suhair and Basheer, Maamon and Maraga, Emad and Cines, Douglas B and Higazi, Abd Al-Roof
Blood, ISSN 0006-4971, 04/2015, Volume 125, Issue 16, pp. 2558 - 2567
Persistent intracerebral hemorrhage (ICH) is amajor cause of death and disability after traumatic brain injury (TBI) for which no medical treatment is... 
RECOMMENDED RESEARCH PRIORITIES | TRANEXAMIC ACID | NATIVE GLU | CLOSED-HEAD INJURY | NERVOUS-SYSTEM | LYS HUMAN-PLASMINOGEN | KNOWLEDGE GAPS | TISSUE | RECEPTOR | HEMATOLOGY | BINDING | Cerebral Hemorrhage - metabolism | Fibrinolysis - drug effects | Tissue Plasminogen Activator - metabolism | Humans | Tranexamic Acid - pharmacology | Brain Injuries - complications | Male | Plasminogen - metabolism | Cerebral Hemorrhage - genetics | Tissue Plasminogen Activator - genetics | Brain - metabolism | Brain - blood supply | Plasminogen Activator Inhibitor 1 - metabolism | Time Factors | Brain Injuries - blood | Plasminogen Activator Inhibitor 1 - genetics | Cerebral Hemorrhage - etiology | Mice, Inbred C57BL | Urokinase-Type Plasminogen Activator - genetics | Mice, Knockout | Animals | Urokinase-Type Plasminogen Activator - metabolism | Antifibrinolytic Agents - pharmacology | Protein Binding | Mutation | Fibrin - metabolism | Thrombosis and Hemostasis
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4. Full Text Epigenetic control of tissue-type plasminogen activator synthesis in human endothelial cells
by Dunoyer-Geindre, Sylvie and Kruithof, Egbert K.O
Cardiovascular Research, ISSN 0008-6363, 06/2011, Volume 90, Issue 3, pp. 457 - 463
Aims Tissue-type plasminogen activator (t-PA) is produced by endothelial cells (EC) and is responsible for the removal of intravascular fibrin deposits. We... 
DNA methylation | Endothelial cell | Histone acetylation | Tissue-type plasminogen activator | LOCALIZATION | WEIBEL-PALADE BODIES | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTEIN-KINASE | T-PA | MESSENGER-RNA LEVELS | GENE PROMOTER | IN-VIVO | GROWTH-FACTOR | HISTONE DEACETYLASE INHIBITORS | EXPRESSION | Promoter Regions, Genetic | Endothelial Cells - metabolism | Humans | RNA, Messenger - genetics | Cells, Cultured | Histone Deacetylases - metabolism | DNA Primers - genetics | Hepatocytes - metabolism | RNA, Messenger - metabolism | Tissue Plasminogen Activator - genetics | DNA Methylation | Tissue Plasminogen Activator - biosynthesis | Base Sequence | Histone Deacetylase Inhibitors - pharmacology | Epigenesis, Genetic - drug effects | Histones - metabolism | Endothelial Cells - drug effects
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5. Full Text Plasminogen Activator Inhibitor-1 Protects Mice Against Cardiac Fibrosis by Inhibiting Urokinase-type Plasminogen Activator-mediated Plasminogen Activation
by Gupta, Kamlesh K and Donahue, Deborah L and Sandoval-Cooper, Mayra J and Castellino, Francis J and Ploplis, Victoria A
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 365 - 11
Plasminogen activator inhibitor-1 (PAI-1) is known to protect mice against cardiac fibrosis. It has been speculated that PAI-1 may regulate cardiac fibrosis by... 
GENETIC DEFICIENCY | TGF-BETA | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | PAI-1 | GENERATION | TISSUES | Gene Expression | Mice, Inbred C57BL | Smad2 Protein - metabolism | Male | Myocardium - pathology | Plasminogen - metabolism | Urokinase-Type Plasminogen Activator - genetics | Heart Diseases - enzymology | Mice, Knockout | Heart Diseases - etiology | Phenotype | Animals | Plasminogen Activator Inhibitor 1 - metabolism | Urokinase-Type Plasminogen Activator - metabolism | Myocardium - metabolism | Fibrosis | Hypertension - complications | Plasminogen Activator Inhibitor 1 - genetics | Fibrinolysin - metabolism | Heart Diseases - pathology | Disease Models, Animal | Heart | Hypertension | Aldosterone | Plasmin | Proenzymes | U-Plasminogen activator | Smad2 protein | Rodents | Plasminogen activator inhibitors | Angiotensin | Angiotensin II | Heart diseases
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6. Full Text RNA Interference-directed Knockdown of Urokinase Plasminogen Activator and Urokinase Plasminogen Activator Receptor Inhibits Prostate Cancer Cell Invasion, Survival, and Tumorigenicity in Vivo
by Sai MuraliKrishna Pulukuri and Christopher S. Gondi and Sajani S. Lakka and Aman Jutla and Norman Estes and Meena Gujrati and Jasti S. Rao
Journal of Biological Chemistry, ISSN 0021-9258, 10/2005, Volume 280, Issue 43, pp. 36529 - 36540
The invasive ability of tumor cells plays a key role in prostate cancer metastasis and is a major cause of treatment failure. Urokinase plasminogen... 
MIGRATION | VITRO | GROWTH-FACTOR-RECEPTOR | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE MODEL | GENE-EXPRESSION | DOWN-REGULATION | UPA PROMOTER | TUMOR-GROWTH | ANTISENSE OLIGONUCLEOTIDES | CATHEPSIN-B | Laminin - pharmacology | Neoplasm Transplantation | Prostatic Neoplasms - metabolism | Cell Proliferation | Humans | Extracellular Matrix - metabolism | Collagen - chemistry | Immunoblotting | Male | Proteoglycans - chemistry | Neoplasm Metastasis | Transfection | RNA Interference | Time Factors | Collagen - pharmacology | Prostatic Neoplasms - pathology | Signal Transduction | Cell Survival | Neoplasm Invasiveness | Electrophoresis, Polyacrylamide Gel | Gene Silencing | Tetrazolium Salts - pharmacology | Urokinase-Type Plasminogen Activator - genetics | Reverse Transcriptase Polymerase Chain Reaction | Plasmids - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Proteoglycans - pharmacology | Urokinase-Type Plasminogen Activator - metabolism | Mice, Nude | Cell Line, Tumor | Laminin - chemistry | Mice | Thiazoles - pharmacology | Neoplasms - pathology | Drug Combinations | Microscopy, Fluorescence | Apoptosis | Mitogen-Activated Protein Kinase 1 - metabolism | RNA, Small Interfering - metabolism | RNAi | uPAR (uPA receptor) | shRNA (small hairpin RNA) | uPA (urokinaseplasminogen activator) | survival | siRNA (small interfering RNA) | prostate cancer | invasion | uPA and uPAR | ANOVA (analysis of variance) | RNAi (RNA interference) | RT (reverse transcription) | TPBS (tween-20 (0.1%) phospate buffered saline) | BSA (bovine serum albumin)
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7. Full Text Human tissue-type plasminogen activator
by Kruithof, Egbert K. O and Dunoyer-Geindre, Sylvie
Thrombosis and Haemostasis, ISSN 0340-6245, 2014, Volume 111, Issue 8, pp. 243 - 254
Summary Tissue-type plasminogen activator (t-PA ) plays an important role in the removal of intravascular fibrin deposits and has several physiological roles... 
Review Article | Nervous system | Plasminogen activators | Gene regulation | Endothelial cells | endothelial cells | PROTEIN-KINASE-C | WEIBEL-PALADE BODIES | RECEPTOR-RELATED PROTEIN | HUMAN-ENDOTHELIAL-CELLS | CAMP-RESPONSIVE ELEMENT | T-PA | VON-WILLEBRAND-FACTOR | nervous system | gene regulation | IN-VIVO | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | CORONARY-HEART-DISEASE | HEMATOLOGY | Gene Expression Regulation, Enzymologic - drug effects | Promoter Regions, Genetic | Transcription, Genetic - drug effects | Genetic Predisposition to Disease | Tissue Plasminogen Activator - metabolism | Humans | Risk Factors | Molecular Sequence Data | Tissue Plasminogen Activator - chemistry | Cardiovascular Diseases - enzymology | Tissue Plasminogen Activator - genetics | Cardiovascular Diseases - genetics | Signal Transduction - drug effects | Base Sequence | Cardiovascular Diseases - epidemiology | Epigenesis, Genetic - drug effects | Protein Processing, Post-Translational
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8. Full Text Urokinase‐type plasminogen activator modulates mammalian circadian clock phase regulation in tissue‐type plasminogen activator knockout mice
by Cooper, Joanna M and Rastogi, Ashutosh and Krizo, Jessica A and Mintz, Eric M and Prosser, Rebecca A and Silver, Rae
European Journal of Neuroscience, ISSN 0953-816X, 03/2017, Volume 45, Issue 6, pp. 805 - 815
Glutamate phase shifts the circadian clock in the mammalian suprachiasmatic nucleus ( SCN ) by activating NMDA receptors. Tissue‐type plasminogen activator (... 
urokinase‐type plasminogen activator | circadian rhythms | suprachiasmatic nucleus | tissue‐type plasminogen activator | urokinase-type plasminogen activator | tissue-type plasminogen activator | NEURONAL MIGRATION | CELL-ADHESION MOLECULE | NEUROTROPHIC FACTOR | RECEPTOR | NEUROSCIENCES | IN-VITRO | EXTRACELLULAR-MATRIX | BIOLOGICAL CLOCK | BRAIN | GENE-FUNCTION | Brain-Derived Neurotrophic Factor - genetics | Suprachiasmatic Nucleus - drug effects | Tissue Plasminogen Activator - metabolism | Mice, Inbred C57BL | Plasminogen Inactivators - pharmacology | Male | Tissue Plasminogen Activator - genetics | Suprachiasmatic Nucleus - physiology | Animals | Urokinase-Type Plasminogen Activator - metabolism | Proteolysis | Circadian Clocks | Female | Suprachiasmatic Nucleus - metabolism | Brain-Derived Neurotrophic Factor - metabolism | Mice | Urokinase | Glutamate | Tissue plasminogen activator | Laws, regulations and rules | Suprachiasmatic nucleus | Glutamic acid | Brain | Night | Glutamic acid receptors (ionotropic) | Brain slice preparation | Nuclei | Plasmin | t-Plasminogen activator | Receptors | Casein | Rodents | Entrainment | Inhibition | Biological clocks | Circadian rhythms | Phase transformations | Phase shift | Polyamide-imides | N-Methyl-D-aspartic acid receptors | Circadian rhythm | Mammals | U-Plasminogen activator | Brain-derived neurotrophic factor | Inhibitors | Plasminogen activator inhibitors | TrkB receptors | Glutamatergic transmission | Gates
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9. Full Text Inactivation of urokinase-type plasminogen activator receptor (uPAR) gene induces dermal and pulmonary fibrosis and peripheral microvasculopathy in mice: a new model of experimental scleroderma?
by Manetti, Mirko and Rosa, Irene and Milia, Anna Franca and Guiducci, Serena and Carmeliet, Peter and Ibba-Manneschi, Lidia and Matucci-Cerinic, Marco
Annals of the Rheumatic Diseases, ISSN 0003-4967, 09/2014, Volume 73, Issue 9, pp. 1700 - 1709
Objective Urokinase-type plasminogen activator receptor (uPAR) is a key component of the fibrinolytic system involved in extracellular matrix remodelling and... 
DIFFERENTIAL EXPRESSION | ANGIOGENESIS | MOUSE MODEL | TISSUE | SCLEROSIS ENDOTHELIAL-CELLS | MECHANISMS | GROWTH-FACTOR | SKIN | RHEUMATOLOGY | SYSTEMIC-SCLEROSIS | CLEAVAGE | Peripheral Vascular Diseases - genetics | Skin - metabolism | Humans | Middle Aged | Scleroderma, Systemic - pathology | Microvessels - pathology | Male | Pulmonary Fibrosis - genetics | Peripheral Vascular Diseases - metabolism | Adult | Female | Skin - pathology | Disease Models, Animal | Myofibroblasts - pathology | Cytokines - metabolism | Mice, Inbred C57BL | Scleroderma, Systemic - metabolism | Scleroderma, Systemic - genetics | Receptors, Urokinase Plasminogen Activator - deficiency | Disease Progression | Mice, Knockout | Receptors, Urokinase Plasminogen Activator - metabolism | Skin - blood supply | Collagen - metabolism | Animals | Biopsy | Fibrosis | Endothelium, Vascular - pathology | Aged | Mice | Receptors, Urokinase Plasminogen Activator - genetics | Peripheral Vascular Diseases - pathology | Apoptosis | Immunohistochemistry | Usage | Care and treatment | Pulmonary fibrosis | Analysis | Thrombolytic drugs | Diagnosis | Alcohol | Studies | Angiogenesis | Lungs | Aqueous solutions | Rodents | Fibroblasts | Scleroderma | Growth factors | Age | Index Medicus
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10. Full Text miR340 suppresses the stem-like cell function of glioma-initiating cells by targeting tissue plasminogen activator
by Yamashita, Daisuke and Kondo, Toru and Ohue, Shiro and Takahashi, Hisaaki and Ishikawa, Madoka and Matoba, Ryo and Suehiro, Satoshi and Kohno, Shohei and Harada, Hironobu and Tanaka, Junya and Ohnishi, Takanori
Cancer Research, ISSN 0008-5472, 03/2015, Volume 75, Issue 6, pp. 1123 - 1133
Glioma-initiating cells (GIC) have stem-like cell properties thought to be sufficient for recurrence, progression, and drug resistance in glioblastomas. In the... 
CANCER-CELLS | MATRIX | INVASION | GENE | ONCOLOGY | HUMAN GLIOBLASTOMA | GROWTH | SELF-RENEWAL | PROLIFERATION | SENESCENCE | DIFFERENTIATION | Cell Proliferation | Neoplasm Invasiveness | Humans | Brain Neoplasms - pathology | Tissue Plasminogen Activator - physiology | Tissue Plasminogen Activator - genetics | Animals | Glioma - pathology | Cell Line, Tumor | Mice | MicroRNAs - physiology | Neoplastic Stem Cells - physiology | Cell Movement
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11. Full Text LRP1 assembles unique co-receptor systems to initiate cell signaling in response to tissue-type plasminogen activator and Myelin-associated glycoprotein
by Mantuano, Elisabetta and Lam, Michael S and Gonias, Steven L
Journal of Biological Chemistry, ISSN 0021-9258, 11/2013, Volume 288, Issue 47, pp. 34009 - 34018
In addition to functioning as an activator of fibrinolysis, tissue-type plasminogen activator (tPA) interacts with neurons and regulates multiple aspects of... 
RECEPTOR-RELATED PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | Protease Inhibitor | BLOOD-BRAIN-BARRIER | NERVE GROWTH-FACTOR | ALPHA-2-MACROGLOBULIN RECEPTOR | NEURITE OUTGROWTH | MEDIATED ACTIVATION | Cell Signaling | Tissue-type Plasminogen Activator (tPA) | MOLECULAR DISSECTION | LONG-TERM POTENTIATION | ERK | Lipoprotein-like Receptor (LRP) | METHYL-D-ASPARTATE | CALCIUM RESPONSES | Disks Large Homolog 4 Protein | Guanylate Kinases - genetics | MAP Kinase Signaling System - physiology | Tissue Plasminogen Activator - metabolism | Humans | Myelin-Associated Glycoprotein - genetics | Myelin-Associated Glycoprotein - metabolism | alpha-Macroglobulins - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Receptors, Nerve Growth Factor - metabolism | Low Density Lipoprotein Receptor-Related Protein-1 - genetics | Tissue Plasminogen Activator - genetics | PC12 Cells | Mitogen-Activated Protein Kinase 1 - genetics | Tumor Suppressor Proteins - genetics | Membrane Proteins - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Lactoferrin - metabolism | Receptors, LDL - genetics | Tumor Suppressor Proteins - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Membrane Proteins - genetics | Low Density Lipoprotein Receptor-Related Protein-1 - metabolism | Rats | Receptors, LDL - metabolism | Nerve Tissue Proteins - genetics | Receptors, Nerve Growth Factor - genetics | Lactoferrin - genetics | Nerve Tissue Proteins - metabolism | alpha-Macroglobulins - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Guanylate Kinases - metabolism | Mice | Mitogen-Activated Protein Kinase 1 - metabolism | Signal Transduction
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