InVivoMAb anti-HIV gp120

Catalog #BE0154
Product Citations:
1
Clone:
55-36
Reactivities:
Virus

$164.00 - $4,280.00

Choose an Option...
  • 100 mg - $4,280.00
  • 50 mg - $3,024.00
  • 25 mg - $2,009.00
  • 5 mg - $600.00
  • 1 mg - $164.00
  • Custom Amount (Quotes Only)
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Product Details

The 55-36 monoclonal antibody reacts with human immunodeficiency virus (HIV) envelope glycoprotein 120 (gp120). gp120 is a 120 kDa glycoprotein exposed on the surface of the HIV envelope. gp120 is essential for virus entry into host cells as it plays a vital role in attachment to DC-SIGN cell surface receptors, sulfate proteoglycan, and CD4. Binding to CD4 induces the start of a cascade of conformational changes in gp120 and gp41 that lead to the fusion of the viral particle with the host cell membrane.

Specifications

Isotype Mouse IgG1, κ
Recommended Isotype Control(s) InVivoMAb mouse IgG1 isotype control, unknown specificity
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Immunogen Recombinant gp120
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <2EU/mg (<0.002EU/μg)
Determined by LAL gel clotting assay
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Production Purified from cell culture supernatant in an animal-free facility
Purification Protein G
RRID AB_10950313
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
    • In Vivo
    • ,
    • Mus musculus (House mouse)
    • ,
    • Cancer Research
    Microbiota triggers STING-type I IFN-dependent monocyte reprogramming of the tumor microenvironment.

    In Cell on 14 October 2021 by Lam, K. C., Araya, R. E., et al.

    PubMed

    The tumor microenvironment (TME) influences cancer progression and therapy response. Therefore, understanding what regulates the TME immune compartment is vital. Here we show that microbiota signals program mononuclear phagocytes in the TME toward immunostimulatory monocytes and dendritic cells (DCs). Single-cell RNA sequencing revealed that absence of microbiota skews the TME toward pro-tumorigenic macrophages. Mechanistically, we show that microbiota-derived stimulator of interferon genes (STING) agonists induce type I interferon (IFN-I) production by intratumoral monocytes to regulate macrophage polarization and natural killer (NK) cell-DC crosstalk. Microbiota modulation with a high-fiber diet triggered the intratumoral IFN-I-NK cell-DC axis and improved the efficacy of immune checkpoint blockade (ICB). We validated our findings in individuals with melanoma treated with ICB and showed that the predicted intratumoral IFN-I and immune compositional differences between responder and non-responder individuals can be transferred by fecal microbiota transplantation. Our study uncovers a mechanistic link between the microbiota and the innate TME that can be harnessed to improve cancer therapies. Published by Elsevier Inc.