The Potent Anti-HIV Protein Cyanovirin-N Contains Two Novel Carbohydrate Binding Sites That Selectively Bind to Man8D1D3 and Man9with Nanomolar Affinity:  Implications for Binding to the HIV Envelope Protein gp120

2001 ◽  
Vol 123 (17) ◽  
pp. 3892-3902 ◽  
Author(s):  
Carole A. Bewley ◽  
Sarah Otero-Quintero
Keyword(s):  
Binding Sites ◽  
Envelope Protein ◽  
Carbohydrate Binding ◽  
Protein Gp120 ◽  
Hiv Envelope ◽  
Anti Hiv ◽  
Envelope Protein Gp120

The HIV Envelope Protein gp120 in the Nervous System

1998 ◽  
Vol 56 (2) ◽  
pp. 153-156 ◽  
Author(s):  
M.Tiziana Corasaniti ◽  
Giacinto Bagetta ◽  
Domenicantonio Rotiroti ◽  
Giuseppe Nisticò
Keyword(s):  
Nervous System ◽  
Envelope Protein ◽  
Protein Gp120 ◽  
Hiv Envelope ◽  
Envelope Protein Gp120

scholarly journals HIV envelope protein gp120-induced apoptosis in lung microvascular endothelial cells by concerted upregulation of EMAP II and its receptor, CXCR3

2014 ◽  
Vol 306 (4) ◽  
pp. L372-L382 ◽  
Author(s):  
Linden A. Green ◽  
Ru Yi ◽  
Daniela Petrusca ◽  
Ting Wang ◽  
Alhasan Elghouche ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Envelope Protein ◽  
Surface Expression ◽  
Endothelial Cell Apoptosis ◽  
Protein Gp120 ◽  
Emap Ii ◽  
Induced Apoptosis ◽  
Hiv Envelope ◽  
Envelope Protein Gp120

Chronic lung diseases, such as pulmonary emphysema, are increasingly recognized complications of infection with the human immunodeficiency virus (HIV). Emphysema in HIV may occur independent of cigarette smoking, via mechanisms that are poorly understood but may involve lung endothelial cell apoptosis induced by the HIV envelope protein gp120. Recently, we have demonstrated that lung endothelial apoptosis is an important contributor to the development of experimental emphysema, via upregulation of the proinflammatory cytokine endothelial monocyte-activating polypeptide II (EMAP II) in the lung. Here we investigated the role of EMAP II and its receptor, CXCR3, in gp120-induced lung endothelial cell apoptosis. We could demonstrate that gp120 induces a rapid and robust increase in cell surface expression of EMAP II and its receptor CXCR3. This surface expression occurred via a mechanism involving gp120 signaling through its CXCR4 receptor and p38 MAPK activation. Both EMAP II and CXCR3 were essentially required for gp120-induced apoptosis and exposures to low gp120 concentrations enhanced the susceptibility of endothelial cells to undergo apoptosis when exposed to soluble cigarette smoke extract. These data indicate a novel mechanism by which HIV infection causes endothelial cell loss involved in lung emphysema formation, independent but potentially synergistic with smoking, and suggest therapeutic targets for emphysema prevention and/or treatment.

scholarly journals Amelioration of Neurotoxic Effects of HIV Envelope Protein gp120 by Fibroblast Growth Factor: A Strategy for Neuroprotection

2001 ◽  
Vol 60 (3) ◽  
pp. 293-301 ◽  
Author(s):  
Ian P. Everall ◽  
Gusta Trillo-Pazos ◽  
Christopher Bell ◽  
Margaret Mallory ◽  
Virginia Sanders ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Envelope Protein ◽  
Fibroblast Growth ◽  
Protein Gp120 ◽  
Neurotoxic Effects ◽  
Hiv Envelope ◽  
Envelope Protein Gp120
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