免疫原 :
Recombinant HIV-1 gp120 Protein (Catalog#11233-V08H)
Antibody Type : Mouse Monoclonal Antibody ( Mouse mAb Service Platform )
克隆号 :
4F4E4
抗体宿主 :
Mouse IgG2b
缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
制备方法 :
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, human cell-derived, recombinant HIV-1 gp120 (rHIV-1 gp120; Catalog#11233-V08H; Ala 29 - Glu 503; 97CN001 strain). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
HIV-1 gp120抗体 Background
Human Immunodeficiency Virus (HIV) can be divided into two major types, HIV type 1 (HIV-1) and HIV type 2 (HIV-2). HIV-1 is related to viruses found in chimpanzees and gorillas living in western Africa. HIV-2 is related to viruses found in sooty mangabeys. HIV-1 viruses may be further divided into groups. The HIV-1 group M viruses predominate and are responsible for the AIDS pandemic. Some of the HIV-1 group M subtypes are known to be more virulent or are resistant to different medications. HIV-2 viruses are thought to be less virulent and transmissible than HIV-1 M group viruses.
The HIV-1 surface protein gp120, also known as Glycoprotein 120, SU, and gp120 is not anchored to the viral envelope, but associates with the extravirion surface through its binding to TM. The surface protein gp120 attaches the virus to the host lymphoid cell by binding to the primary receptor CD4. This interaction induces a structural rearrangement creating a high affinity binding site for a chemokine coreceptor like CXCR4 and/or CCR5. Surface protein gp120 is a ligand for CD209 / DC-SIGN and CLEC4M / DC-SIGNR. It may target the virus to gut-associated lymphoid tissue (GALT) by binding host ITGA4/ITGB7 (alpha-4/beta-7 integrins), a complex that mediates T-cell migration to the GALT. Interaction between gp120 and ITGA4/ITGB7 would allow the virus to enter GALT early in the infection, infecting and killing most of GALT's resting CD4+ T-cells. This T-cell depletion is believed to be the major insult to the host immune system leading to AIDS.
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