about
Infantile Hemangioma Originates From A Dysregulated But Not Fully Transformed Multipotent Stem Cell.Nonenzymatic interactions between proteinases and the cell surface: novel roles in normal and malignant cell physiology.Control of type IV collagenase activity by components of the urokinase-plasmin system: a regulatory mechanism with cell-bound reactants.Membrane-Type 1 Matrix Metalloproteinase Downregulates Fibroblast Growth Factor-2 Binding to the Cell Surface and Intracellular Signaling.TIMP-2 Interaction with MT1-MMP Activates the AKT Pathway and Protects Tumor Cells from ApoptosisUrokinase Receptor Promotes Skin Tumor Formation by Preventing Epithelial Cell Activation of Notch1.Elevated expression of periostin in human osteoarthritic cartilage and its potential role in matrix degradation via matrix metalloproteinase-13.In vitro angiogenesis on the human amniotic membrane: requirement for basic fibroblast growth factor-induced proteinases.Differential modulation of cell phenotype by different molecular weight forms of basic fibroblast growth factor: possible intracellular signaling by the high molecular weight forms.Basic fibroblast growth factor (FGF-2): the high molecular weight forms come of age.Vascular injury and modulation of MAPKs: a targeted approach to therapy of restenosis.Inhibition of smooth muscle cell migration and neointima formation in vein grafts by overexpression of matrix metalloproteinase-3.Basic fibroblast growth factor released by single, isolated cells stimulates their migration in an autocrine mannerMitral valve prolapse is associated with altered extracellular matrix gene expression patterns.Inhibition of Breast Cancer Metastasis by Presurgical Treatment with an Oral Matrix Metalloproteinase Inhibitor: A Preclinical Proof-of-Principle Study.Arrested Development: Infantile Hemangioma and the Stem Cell Teratogenic Hypothesis.Shedding of membrane vesicles mediates fibroblast growth factor-2 release from cells.Biology and biochemistry of proteinases in tumor invasion.Plasminogen activators and angiogenesis.TGF-beta1 induces rearrangement of FLK-1-VE-cadherin-beta-catenin complex at the adherens junction through VEGF-mediated signaling.TGF-β1 induces endothelial cell apoptosis by shifting VEGF activation of p38(MAPK) from the prosurvival p38β to proapoptotic p38α.Transforming growth factor-beta 1 (TGF-beta1) induces angiogenesis through vascular endothelial growth factor (VEGF)-mediated apoptosis.Basic fibroblast growth factor, a protein devoid of secretory signal sequence, is released by cells via a pathway independent of the endoplasmic reticulum-Golgi complex.New observations on the intracellular localization and release of bFGF.Thrombin cleaves the high molecular weight forms of basic fibroblast growth factor (FGF-2): a novel mechanism for the control of FGF-2 and thrombin activity.Activation of progelatinase A (MMP-2) by neutrophil elastase, cathepsin G, and proteinase-3: a role for inflammatory cells in tumor invasion and angiogenesis.Activation of mitogen-activated protein kinases during preparation of vein grafts and modulation by a synthetic inhibitor.Modulation of matrix metalloproteinase activity in human saphenous vein grafts using adenovirus-mediated gene transfer.Vein graft arterialization causes differential activation of mitogen-activated protein kinases.PDGF-BB induces vascular smooth muscle cell expression of high molecular weight FGF-2, which accumulates in the nucleus.Soluble factor(s) released from neutrophils activates endothelial cell matrix metalloproteinase-2.Urokinase plasminogen activator and gelatinases are associated with membrane vesicles shed by human HT1080 fibrosarcoma cells.Topical mitogen-activated protein kinases inhibition reduces intimal hyperplasia in arterialized vein grafts.Tumor cells secrete an angiogenic factor that stimulates basic fibroblast growth factor and urokinase expression in vascular endothelial cells.Mechanisms of c-reactive protein up-regulation in arterialized vein grafts.Plasmin activates pro-matrix metalloproteinase-2 with a membrane-type 1 matrix metalloproteinase-dependent mechanismMatrix Metalloproteinase Inhibitors in Cancer Therapy: Turning Past Failures Into Future SuccessesA quantitative in vitro model of smooth muscle cell migration through the arterial wall using the human amniotic membraneThe role of proteases in matrix breakdown during cellular invasionPurification and biological activities of an angiogenesis factor from human placenta
P50
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P50
description
hulumtues
@sq
researcher
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wetenschapper
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հետազոտող
@hy
name
Paolo Mignatti
@ast
Paolo Mignatti
@en
Paolo Mignatti
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Paolo Mignatti
@nl
Paolo Mignatti
@sl
type
label
Paolo Mignatti
@ast
Paolo Mignatti
@en
Paolo Mignatti
@es
Paolo Mignatti
@nl
Paolo Mignatti
@sl
prefLabel
Paolo Mignatti
@ast
Paolo Mignatti
@en
Paolo Mignatti
@es
Paolo Mignatti
@nl
Paolo Mignatti
@sl
P106
P21
P31
P496
0000-0002-8157-457X