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The primary role of the S(52,56) residues of Vpu in antagonism of CD4, GaLV Env, and BST-2/tetherin is to recruit the SCF/betaTrCP ubiquitin ligase.
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Studied role of bone marrow stromal cell antigen 2 (BST2) in gastric cancer (GC); results show BST2 is overexpressed in GC tissues and BST2 silencing inhibits cell proliferation and migration, partly by regulating NF-kappaB signaling.
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The results establish tetherin as a key effector of the intrinsic immune defense against HIV-1, and they demonstrate that Vpu-mediated tetherin antagonism is critical for efficient viral spread during the initial phase of HIV-1 replication.
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findings support the notion that NAbs can induce ADCC. They highlight that while BST2 antagonism by HIV promotes ADCC evasion, strategies aimed at restoring BST2 restriction could improve anti-HIV responses and potentially provide a means to eliminate reactivated cells in latent reservoirs.
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BST2 likely mediates platinum resistance in nasopharyngeal cancer via NF-kappaB signaling
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These data collectively suggest that the human parainfluenza virus type 2 V protein inhibits tetherin expression induced by several external stimuli.
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These results suggest that tetherin antagonism by V proteins is common among the genus Rubulavirus.
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High BST2 expression is associated with Esophageal, Gastric, or Colorectal Cancer.
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Two additional regulators of BST2 constitutive ubiquitylation and sorting to the lysosomes: the E3 ubiquitin ligases NEDD4 and MARCH8, are reported.
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Coimmunoprecipitation studies indicated that non-glycosylated tetherin is stabilized through the formation of a ternary SGTA/Vpu/tetherin complex. Although the results do not provide support for a physiological function of SGTA in HIV-1 replication, they demonstrate that SGTA overexpression regulates tetherin expression and stability, thus providing insights into the function of SGTA in endoplasmic reticulum translocation
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Importantly, the authors demonstrate for the first time that the HIV-2 Env induces NF-kappaB activation in HEKappa293T cells. Furthermore, the anti-BST-2 activity of the HIV-2 Env is not sufficient to completely inhibit NF-kappaB activity.
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Data revealed that under a nutrient deficient condition, CD317 functions as an anti-apoptotic factor through AIF-mediated caspase and autophagy-independent manner.
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findings lead us to believe that BISPR and BST2 may regulate egress of HEV virions into bile in vivo. This system may also be used to scale up virus production in vitro
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a non-canonical autophagy pathway reminiscent of LC3-associated phagocytosis contributes to Vpu counteraction of BST2 restriction.
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Ebola virus GP1,2, the Ebola virus matrix protein VP40, and BST2 are at least additive with respect to the induction of NF-kappaB activity.
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Studied the mechanism of viral budding and tethering mediated by human BST-2/tetherin using a model of BST-2 embedded in a membrane and used steered molecular dynamics to simulate the transition from the host cell membrane associated form to the cell-virus membrane bridging form.
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Disruption of BST-2 dimerization offers a potential therapeutic approach for breast cancer.
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identified WDR81 as a novel gene required for tetherin trafficking and degradation in both the presence and absence of Vpu
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Among 32 HIV-2 ROD Env mutants tested, the authors demonstrated that the asparagine residue at position 659 located in the gp36 ectodomain is mandatory to exert the anti-tetherin function.
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Despite the influence of rs919266 and rs9576 on BST2 expression being still undetermined, a preventive role by BST2 polymorphisms was found during HIV-1 infection.
