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Envelope surface glycoprotein gp120
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env
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HIV-1 ADA, IIIB, and MN Env (gp120) binds to TUBB3 (tubulin beta-3), which can be inhibited by a small peptide (Helix-A) derived from gp120 |
PubMed
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Envelope surface glycoprotein gp160, precursor
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env
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Treatment of cells with actin-depolymerizing agents or tubulin polymerization inhibitors largely reduces the percentage of cells with capped HIV-1 Gag and Env, indicating an intact actin and tubulin cytoskeleton is required for efficient assembly of HIV-1 |
PubMed
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Pr55(Gag)
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gag
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Treatment of cells with actin-depolymerizing agents or tubulin polymerization inhibitors largely reduces the percentage of cells with capped HIV-1 Gag and Env, indicating an intact actin and tubulin cytoskeleton is required for efficient assembly of HIV-1 |
PubMed
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Rev
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rev
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HIV-1 Rev interacting protein, TUBB3, is identified by the in-vitro binding experiments involving cytosolic or nuclear extracts from HeLa cells |
PubMed
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rev
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Rev acts to depolymerize microtubules that are formed by tubulin, an effect that is observed during HIV-1 infection |
PubMed
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Tat
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tat
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HIV-1 Tat K29A, K50R, and K51R lysine mutations downregulate the proportion of soluble tubulin in cells, while the majority of other lysine mutations upregulate the percentage of soluble tubulin compared with the wild-type |
PubMed
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tat
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In Jurkat cells expressing HIV-1 Tat, decreased expression levels are found for basic cytoskeletal proteins such as actin, beta-tubulin, annexin, cofilin, gelsolin, and Rac/Rho-GDI complex |
PubMed
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tat
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HIV-1 Tat (specifically, amino acids 38-72), enhances tubulin polymerization and triggers the mitochondrial pathway to induce T cell apoptosis as shown in vitro by the release of cytochrome c from isolated mitochondria |
PubMed
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tat
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HIV-1 Tat (amino acids 36-39) binds tubulin alpha/beta dimers and polymerized microtubules leading to the alteration of microtubule dynamics and activation of a mitochondria-dependent apoptotic pathway that is facilitated by the Bcl-2 relative Bim |
PubMed
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Vpr
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vpr
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Concurrent exposure of HIV-1 Vpr with HCV core protein causes significantly increased human fetal neuron (HFN) injury, as indicated by reduced beta-III-tubulin, than HFN treated with HIV-1 Vpr alone |
PubMed
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