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AB63996

Recombinant HIV1 Nef protein

Recombinant HIV1 Nef protein

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(2 Publications)

Recombinant HIV1 Nef protein is a Human immunodeficiency virus type 1 (BRU ISOLATE) Full Length protein, in the 1 to 206 aa range, expressed in Escherichia coli, with >90%, suitable for SDS-PAGE.

別名を表示する

Protein Nef, 3'ORF, Negative factor, F-protein, nef

1 Images
SDS-PAGE - Recombinant HIV1 Nef protein (AB63996)
  • SDS-PAGE

Unknown

SDS-PAGE - Recombinant HIV1 Nef protein (AB63996)

Polyacrylamide gel electrophoresis of ab63996.

Key facts

精製度

>90% SDS-PAGE

発現系

Escherichia coli

タグ

Tag free

アプリケーション

SDS-PAGE

applications

生物活性

No

アクセッション番号

P03406

アニマルフリー

No

キャリアフリー

No

Human immunodeficiency virus type 1 (BRU ISOLATE)

バッファー組成

pH: 6 - 8.5 Constituents: 50% Glycerol (glycerin, glycerine), 0.316% Tris HCl, 0.29% Sodium chloride, 0.078% 2-Mercaptoethanol

storage-buffer

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }

製品の詳細

ab63996 has been derived from infectious plasmid clone pNL4-3 and belongs to Group B of HIV-1.

配列情報

[{"sequence":"MGGKWSKSSVVGWPTVRERMRRAEPAADGVGAASRDLEKHGAITSSNTAATNAACAWLEAQEEEEVGFPVTPQVPLRPMTYKAAVDLSHFLKEKGGLEGLIHSQRRQDILDLWIYHTQGYFPDWQNYTPGPGVRYPLTFGWCYKLVPVEPDKVEEANKGENTSLLHPVSLHGMDDPEREVLEWRFDSRLAFHHVARELHPEYFKNC","proteinLength":"Full Length","predictedMolecularWeight":null,"actualMolecularWeight":null,"aminoAcidEnd":206,"aminoAcidStart":1,"nature":"Recombinant","expressionSystem":"Escherichia coli","accessionNumber":"P03406","tags":[]}]

出荷温度及び保存条件

出荷温度
Blue Ice
短期保存温度
-20°C
長期保存温度
-20°C
分注に関する情報
Upon delivery aliquot
保管に関する情報
Avoid freeze / thaw cycle
False

補足情報

This supplementary information is collated from multiple sources and compiled automatically.

HIV1 Nef also known as Nef HIV Nef protein and Nef HIV protein is a small myristoylated protein with a mass of approximately 27 kDa. It expresses predominantly in the cytoplasm of HIV-1 infected cells. HIV1 Nef plays an important role in viral pathogenicity by manipulating host cell machinery to favor viral replication and immune escape. The protein affects the host cell's plasma membrane and endosomal compartments where it modifies the trafficking of various cell surface molecules.
Biological function summary

Nef affects several cellular processes to promote viral persistence and disease progression. It disrupts normal cellular signaling and acts as part of larger protein complexes that interact with host proteins. For instance it is known for its interaction with proteins like AP-1 which Nef uses to alter the re-routing of MHC-I molecules to lysosomes. This results in reduced exposure of infected cells to the immune system and highlights its role in immune evasion.

Pathways

Nef engages in interference with immune and cellular signaling pathways. It tightly interacts with the PI3K/Akt signaling pathway important for cell survival and proliferation thereby assisting the virus in sustaining a hospitable cellular environment. Nef also partners with Src family kinases further supporting its functions in reprogramming cellular processes and enhancing viral replication.

HIV1 Nef is intimately related to HIV/AIDS pathogenesis. It contributes significantly to the immunodeficiency observed in infected individuals by modulating CD4 and CTLA-4 downmodulation affecting immune signaling and response. Furthermore Nef aligns with Tat protein in HIV-infected cells enhancing the pathological effects seen in the neurodysfunction often associated with disease progression illustrating its role in complex interactions that worsen HIV-related complications.

製品の性状

製品の状態

Liquid

補足情報

Highly purified by several steps of chromatography.

一般的な情報

機能

Factor of infectivity and pathogenicity, required for optimal virus replication (PubMed : 8151761). Alters numerous pathways of T-lymphocytes function and down-regulates immunity surface molecules in order to evade host defense and increase viral infectivity (PubMed : 25585010). Alters the functionality of other immunity cells, like dendritic cells, monocytes/macrophages and NK cells (PubMed : 25585010).. In infected CD4(+) T-lymphocytes, down-regulates the surface MHC-I, mature MHC-II, CD4, CD28, CCR5 and CXCR4 molecules. Mediates internalization and degradation of host CD4 through the interaction of with the cytoplasmic tail of CD4, the recruitment of AP-2 (clathrin adapter protein complex 2), internalization through clathrin coated pits, and subsequent transport to endosomes and lysosomes for degradation. Diverts host MHC-I molecules to the trans-Golgi network-associated endosomal compartments by an endocytic pathway to finally target them for degradation. MHC-I down-regulation may involve AP-1 (clathrin adapter protein complex 1) or possibly Src family kinase-ZAP70/Syk-PI3K cascade recruited by PACS2. In consequence infected cells are masked for immune recognition by cytotoxic T-lymphocytes. Decreasing the number of immune receptors also prevents reinfection by more HIV particles (superinfection). Down-regulates host SERINC3 and SERINC5 thereby excluding these proteins from the viral particles. Virion infectivity is drastically higher when SERINC3 or SERINC5 are excluded from the viral envelope, because these host antiviral proteins impair the membrane fusion event necessary for subsequent virion penetration.. Bypasses host T-cell signaling by inducing a transcriptional program nearly identical to that of anti-CD3 cell activation. Interaction with TCR-zeta chain up-regulates the Fas ligand (FasL) (By similarity). Increasing surface FasL molecules and decreasing surface MHC-I molecules on infected CD4(+) cells send attacking cytotoxic CD8+ T-lymphocytes into apoptosis (PubMed : 11298454).. Plays a role in optimizing the host cell environment for viral replication without causing cell death by apoptosis. Protects the infected cells from apoptosis in order to keep them alive until the next virus generation is ready to strike. Inhibits the Fas and TNFR-mediated death signals by blocking MAP3K5/ASK1. Decreases the half-life of TP53, protecting the infected cell against p53-mediated apoptosis. Inhibits the apoptotic signals regulated by the Bcl-2 family proteins through the formation of a Nef/PI3-kinase/PAK2 complex that leads to activation of PAK2 and induces phosphorylation of host BAD.. Extracellular Nef protein targets CD4(+) T-lymphocytes for apoptosis by interacting with CXCR4 surface receptors (PubMed : 14990729).

配列の類似性

Belongs to the lentivirus primate group Nef protein family.

翻訳後修飾

The virion-associated Nef proteins are cleaved by the viral protease to release the soluble C-terminal core protein. Nef is probably cleaved concomitantly with viral structural proteins on maturation of virus particles.. Myristoylated.. Phosphorylated on serine residues, probably by host PKCdelta and theta.

製品プロトコール

ターゲットの情報

Factor of infectivity and pathogenicity, required for optimal virus replication (PubMed : 8151761). Alters numerous pathways of T-lymphocytes function and down-regulates immunity surface molecules in order to evade host defense and increase viral infectivity (PubMed : 25585010). Alters the functionality of other immunity cells, like dendritic cells, monocytes/macrophages and NK cells (PubMed : 25585010).. In infected CD4(+) T-lymphocytes, down-regulates the surface MHC-I, mature MHC-II, CD4, CD28, CCR5 and CXCR4 molecules. Mediates internalization and degradation of host CD4 through the interaction of with the cytoplasmic tail of CD4, the recruitment of AP-2 (clathrin adapter protein complex 2), internalization through clathrin coated pits, and subsequent transport to endosomes and lysosomes for degradation. Diverts host MHC-I molecules to the trans-Golgi network-associated endosomal compartments by an endocytic pathway to finally target them for degradation. MHC-I down-regulation may involve AP-1 (clathrin adapter protein complex 1) or possibly Src family kinase-ZAP70/Syk-PI3K cascade recruited by PACS2. In consequence infected cells are masked for immune recognition by cytotoxic T-lymphocytes. Decreasing the number of immune receptors also prevents reinfection by more HIV particles (superinfection). Down-regulates host SERINC3 and SERINC5 thereby excluding these proteins from the viral particles. Virion infectivity is drastically higher when SERINC3 or SERINC5 are excluded from the viral envelope, because these host antiviral proteins impair the membrane fusion event necessary for subsequent virion penetration.. Bypasses host T-cell signaling by inducing a transcriptional program nearly identical to that of anti-CD3 cell activation. Interaction with TCR-zeta chain up-regulates the Fas ligand (FasL) (By similarity). Increasing surface FasL molecules and decreasing surface MHC-I molecules on infected CD4(+) cells send attacking cytotoxic CD8+ T-lymphocytes into apoptosis (PubMed : 11298454).. Plays a role in optimizing the host cell environment for viral replication without causing cell death by apoptosis. Protects the infected cells from apoptosis in order to keep them alive until the next virus generation is ready to strike. Inhibits the Fas and TNFR-mediated death signals by blocking MAP3K5/ASK1. Decreases the half-life of TP53, protecting the infected cell against p53-mediated apoptosis. Inhibits the apoptotic signals regulated by the Bcl-2 family proteins through the formation of a Nef/PI3-kinase/PAK2 complex that leads to activation of PAK2 and induces phosphorylation of host BAD.. Extracellular Nef protein targets CD4(+) T-lymphocytes for apoptosis by interacting with CXCR4 surface receptors (PubMed : 14990729).
See full target information nef

文献 (2)

Recent publications for all applications. Explore the full list and refine your search

Journal of extracellular vesicles 13:e12478 PubMed39016173

2024

HIV-1 Nef is carried on the surface of extracellular vesicles.

Applications

Unspecified application

Species

Unspecified reactive species

Christophe Vanpouille,Beda Brichacek,Tatiana Pushkarsky,Larisa Dubrovsky,Wendy Fitzgerald,Nigora Mukhamedova,Sofia Garcia-Hernandez,Doreen Matthies,Anastas Popratiloff,Dmitri Sviridov,Leonid Margolis,Michael Bukrinsky

Journal of neuroinflammation 21:127 PubMed38741181

2024

Extracellular vesicles produced by HIV-1 Nef-expressing cells induce myelin impairment and oligodendrocyte damage in the mouse central nervous system.

Applications

Unspecified application

Species

Unspecified reactive species

Jessica K Schenck,Molly T Karl,Cheryl Clarkson-Paredes,Ashley Bastin,Tatiana Pushkarsky,Beda Brichacek,Robert H Miller,Michael I Bukrinsky
View all publications

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