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|Cat. #||Product Name||Price|
|H09275||GP120 - W61D - 99||Inquiry|
|H09017||GP120 - W61D - 98 - S||Inquiry|
|H09619||GP120 - W61D - 98||Inquiry|
|H09023||GP120 - W61D - 97 - S||Inquiry|
|H09305||GP120 - W61D - 97||Inquiry|
|H09394||GP120 - W61D - 96||Inquiry|
|H09533||GP120 - W61D - 95||Inquiry|
|H09067||GP120 - W61D - 94||Inquiry|
|H09198||GP120 - W61D - 93||Inquiry|
|H09128||GP120 - W61D - 92||Inquiry|
|H09137||GP120 - W61D - 91||Inquiry|
|H09553||GP120 - W61D - 90||Inquiry|
|H09537||GP120 - W61D - 9||Inquiry|
|H09518||GP120 - W61D - 89||Inquiry|
|H09517||GP120 - W61D - 88||Inquiry|
The molecular weight of Env protein is 160 KD, so it is also called gp160. The initially synthesized Env is aggregated in the endoplasmic reticulum, then transferred to Golgi for glycosylation, and then cut into two smaller proteins, gp41 and gp120, by proteases in the cells. Gp41 contains the transmembrane region of Env, which is deeply located in the lipid bilayer of the newly synthesized toxic particles, while gp120 is located on the surface of the toxic particles and infected cells, and connects with gp41 by non-covalent bond. The whole Env protein exists in the form of trimer on the surface of toxic particles and infected cells.
Mechanism of GP120 in HIV
In order to invade nerve cells, the HIV virus first needs the binding of its envelope glycoprotein gp120 to CD4 molecules. After binding to the CD4 molecule, the conformation of gp120 changes, resulting in the exposure of the conserved region which was previously folded into the core structure. Gp120 then binds to the co-receptor CCR5 or CXCR4 to change the conformation of gp41, which mediates the fusion of the virus with the cell and enters the cell. Compared with CD4+T cells in peripheral blood, the level of CD4 molecules on the surface of nerve cells is much lower. In order to adapt to the microenvironment in the brain, the dependence of HIV on CD4 molecules has changed. Studies have shown that the frequency of CD4-dependent HIV envelope glycoprotein Envs in the brain of patients with AIDS dementia syndrome is significantly higher than that of peripheral tissues such as lymph and blood. At the same time, Julio Martin et al. found that the dependence of HIV isolates from peripheral blood on CD4 was also decreased when the recombinant viruses were packaged after adapting to the microglia microenvironment in vitro.
When HIV-1 evolves in the brain, its envelope glycoprotein gp120 gene mutation can reduce the dependence of HIV-1 on CD4 receptor and CXCR4 co-receptor, and enhance its use of CCR5 co-receptor. HIV-1 gp120 can damage nerve cells not only directly, but also indirectly. Gp120 mainly causes nervous system injury through NMDA receptor-mediated excitatory poisoning, activation of apoptosis process and activation of chemokine receptors/inflammatory factors. Therefore, it is necessary to study the role of Gp120 in the pathogenesis of AIDS dementia syndrome.
1. Hioe, C. E., Tuen, M., Chien, P. C., Jones, G., Ratto-Kim, S., Norris, P. J., ... & Zolla-Pazner, S. (2001). Inhibition of human immunodeficiency virus type 1 gp120 presentation to CD4 T cells by antibodies specific for the CD4 binding domain of gp120. Journal of virology, 75(22), 10950-10957.
2. Haynes, B. F., Liao, H. X., Tomaras, G., Kepler, T. B., Hwang, K. K., Alam, S. M., ... & Bonsignori, M. (2016). U.S. Patent Application No. 15/056,655.