Monocyte chemotactic activity in human abdominal aortic aneurysms: Role of elastin degradation peptides and the 67–kD cell surface elastin receptor

This publication has 43 references indexed in Scilit:

• Decreased Elastin Deposition and High Proliferation of Fibroblasts from Costello Syndrome Are Related to Functional Deficiency in the 67-kD Elastin-Binding Protein
  The American Journal of Human Genetics, 2000
• Differentiation of U937 Cells Enables a Phospholipase D-Dependent Pathway of Cytosolic Phospholipase A2 Activation
  Biochemical and Biophysical Research Communications, 1999
• Recycling of the 67-kDa Elastin Binding Protein in Arterial Myocytes Is Imperative for Secretion of Tropoelastin
  Experimental Cell Research, 1995
• Inflammation and Matrix Metalloproteinases in the Enlarging Abdominal Aortic Aneurysm
  Arteriosclerosis, Thrombosis, and Vascular Biology, 1995
• Effect of Elastin Peptides on Vascular Tone
  Journal of Vascular Research, 1995
• Migration of monocytes in the presence of elastolytic fragments of elastin and in synthetic derivates Structure‐activity relationships
  International Journal of Peptide and Protein Research, 1994
• Nature and the Multiple Functions of the 67-kD Elastin-/Laminin Binding Protein
  Cell Adhesion and Communication, 1994
• Peptide sequences selected by BA4, a tropoelastin-specific monoclonal antibody, are ligands for the 67-kilodalton bovine elastin receptor
  Biochemistry, 1993
• Ligand affinity of the 67-kD elastin/laminin binding protein is modulated by the protein's lectin domain: visualization of elastin/laminin-receptor complexes with gold-tagged ligands.
  Journal of Cell Biology, 1991
• Chemotactic responses of fibroblasts to tropoelastin and elastin-derived peptides.
  Journal of Clinical Investigation, 1982