Mouse Anti-HIV-1 gp120 Recombinant Antibody (CBMW-H0767) (CBMAB-V208-0871-FY)

Name: Mouse Anti-HIV-1 gp120 Recombinant Antibody (CBMW-H0767)
SKU: CBMAB-V208-0871-FY
Rating: 5 (1 reviews)

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Datasheet

SDS

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Basic Information

Host Animal

Mouse

Clone

CBMW-H0767

Application

ELISA, IF, WB

Immunogen

Raised in mouse using HIV1 gp120

Specificity

HIV

Antibody Isotype

IgG2a

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

PBS, pH 7.2

Preservative

0.1% Sodium azide

Concentration

0.1 mg/mL

Purity

>90% by SDS-PAGE

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at-20°C long term. Avoid repeated freeze/thaw cycles.

More Infomation

Target

Full Name

Envelope glycoprotein GP120

Introduction

The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).

Entrez Gene ID

155971

UniProt ID

P04578

Alternative Names

Human immunodeficiency virus type 1; HIV-1; Envelope glycoprotein GP120; gp120; HIV envelope

Function

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. Acts as a ligand for CD209/DC-SIGN and CLEC4M/DC-SIGNR, which are respectively found on dendritic cells (DCs), and on endothelial cells of liver sinusoids and lymph node sinuses. These interactions allow capture of viral particles at mucosal surfaces by these cells and subsequent transmission to permissive cells. HIV subverts the migration properties of dendritic cells to gain access to CD4+ T-cells in lymph nodes. Virus transmission to permissive T-cells occurs either in trans (without DCs infection, through viral capture and transmission), or in cis (following DCs productive infection, through the usual CD4-gp120 interaction), thereby inducing a robust infection. In trans infection, bound virions remain infectious over days and it is proposed that they are not degraded, but protected in non-lysosomal acidic organelles within the DCs close to the cell membrane thus contributing to the viral infectious potential during DCs' migration from the periphery to the lymphoid tissues. On arrival at lymphoid tissues, intact virions recycle back to DCs' cell surface allowing virus transmission to CD4+ T-cells.

Biological Process

Actin filament reorganization Source: UniProtKB-UniRule
Clathrin-dependent endocytosis of virus by host cell Source: UniProtKB
Fusion of virus membrane with host endosome membrane Source: UniProtKB-UniRule
Fusion of virus membrane with host plasma membrane Source: UniProtKB
Mitigation of host immune response by virus Source: UniProtKB-UniRule
Positive regulation of establishment of T cell polarity Source: UniProtKB-UniRule
Positive regulation of plasma membrane raft polarization Source: UniProtKB-UniRule
Positive regulation of receptor clustering Source: UniProtKB-UniRule
Viral protein processing Source: UniProtKB
Virion attachment to host cell Source: UniProtKB

Cellular Location

Virion membrane; Host cell membrane; Host endosome membrane. The surface protein is not anchored to the viral envelope, but associates with the extravirion surface through its binding to TM. It is probably concentrated at the site of budding and incorporated into the virions possibly by contacts between the cytoplasmic tail of Env and the N-terminus of Gag.

PTM

Highly glycosylated by host. The high number of glycan on the protein is reffered to as 'glycan shield' because it contributes to hide protein sequence from adaptive immune system.
Palmitoylation of the transmembrane protein and of Env polyprotein (prior to its proteolytic cleavage) is essential for their association with host cell membrane lipid rafts. Palmitoylation is therefore required for envelope trafficking to classical lipid rafts, but not for viral replication.
Specific enzymatic cleavages in vivo yield mature proteins. Envelope glycoproteins are synthesized as a inactive precursor that is heavily N-glycosylated and processed likely by host cell furin in the Golgi to yield the mature SU and TM proteins. The cleavage site between SU and TM requires the minimal sequence [KR]-X-[KR]-R. About 2 of the 9 disulfide bonds of gp41 are reduced by P4HB/PDI, following binding to CD4 receptor.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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