|PUBLICATIONS (Ranked by impact factor of the journal)|
Phospholipase D Is a Central Regulator of Collagen I-Induced Cytoskeletal Rearrangement and Podosome Formation in Megakaryocytes|
Podosome formation, spreading and ultra-structure of phospholipase D single- and double-deficient megakaryocytes were analyzed using confocal and transmission electron microscopy. [J Thromb Haemost] Abstract
Cell-Specific and Endothelium-Dependent Regulations of Matrix Metalloproteinase-2 in Rat Aorta
Scientists studied signaling mechanisms employed by angiotensin II in the regulation of latent (pro-) and active forms of matrix metalloproteinase-2 in rat aortic endothelial and smooth muscle cells, along with isolated rat aorta. [Basic Res Cardiol] Abstract
Defective Collagen VI α6 Chain Expression in the Skeletal Muscle of Patients with Collagen VI-Related Myopathies
The collagen VI α6 chain is a recently identified component of the extracellular matrix of the human skeletal muscle. Researchers report that the α6 chain was dramatically reduced in skeletal muscle and muscle cell cultures of genetically characterized Ullrich congenital muscular dystrophy, Bethlem myopathy and myosclerosis myopathy patients, independently of the clinical phenotype, the gene involved and the effect of the mutation on the expression of the “classical” α1α2α3 heterotrimer. [Biochim Biophys Acta] Full Article
Expression and Y435-Phosphorylation of Abelson Interactor 1 (Abi1) Promotes Tumor Cell Adhesion, Extracellular Matrix Degradation and Invasion by Colorectal Carcinoma Cells
The specific role of Abi1 in relation to extracellular matrix degradation and effects of targeting Abi1 phosphorylation have not yet been examined. Researchers investigated the role of Abi1 in relation to invasive properties in colorectal cancer. [Mol Cancer] Abstract
Up-Regulated HMGB1 in EAM Directly Led to Collagen Deposition by a PKCβ/Erk1/2-Dependent Pathway: Cardiac Fibroblast/Myofibroblast Might Be Another Source of HMGB1
Investigators assessed whether up-regulated high mobility group box 1 (HMGB1) could directly lead to cardiac fibrosis in experimental autoimmune myocarditis (EAM); cardiac fibroblast/myofibroblasts could secrete HMGB1 as another source of high-level HMGB1 in EAM; and HMGB1 blockade could effectively prevent cardiac fibrosis at the last stage of EAM. [J Cell Mol Med] Full Article
Constitutive Nuclear Expression of Dentin Matrix Protein 1 Fails to Rescue the Dmp1-Null Phenotype
For gene expression comparisons, using an adenovirus construct, scientists targeted the expressions of dentin matrix protein 1 (DMP1) either to the nucleus only by replacing the endogenous signal peptide with a nuclear localization signal sequence, or to the extracellular matrix as the WT type in MC3T3 osteoblasts for gene expression comparisons. [J Biol Chem] Abstract
Involvement of Matrix Metalloproteinase-9 in Amyloid-β 1-42-Induced Shedding of the Pericyte Proteoglycan NG2
To understand the cellular events underlying amyloid-β (Aβ)1-42 effects on microvascular alterations, researchers investigated whether different aggregation forms of Aβ1-42 affect shedding of the pericyte proteoglycan NG2 and whether they affect proteolytic cleavage mediated by matrix metalloproteinase-9. [J Neuropathol Exp Neurol] Abstract
Pericellular Proteolysis by Matrix Metalloproteinase-7 Is Differentially Modulated by Cholesterol Sulfate, Sulfatide and Cardiolipin
Matrix metalloproteinase-7 (MMP-7) potentially associates with cell surface via sulfatide and cardiolipin when they are overexpressed on the cell surface. Scientists investigated the molecular interaction between these acidic lipids and MMP-7 or its substrates, and their effects on the activity of MMP-7. [FEBS J] Abstract
Laminin α2-Mediated Focal Adhesion Kinase Activation Triggers Alport Glomerular Pathogenesis
Scientists showed that laminins containing the α2 chain, but not those containing the α1 chain activates focal adhesion kinase on glomerular podocytes in vitro and in vivo. [PLoS One] Full Article
Uridine 5′-Triphosphate Promotes In Vitro Schwannoma Cell Migration through Matrix Metalloproteinase-2 Activation
Researchers found that uridine 5′-triphosphate treatment induced Schwannoma cell migration through activation of P2Y2 receptors and through the increase of extracellular matrix metalloproteinase-2 activation and expression. [PLoS One] Full Article
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