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The cytoplasmic domain of HIV-1 Vpu contributes to the physical interaction with, and functional antagonism of chimpanzee BST-2.
Bovine tetherinb (bST2A1) blocks retrovirus release, however, has no effect on cell-to-cell transmission of retroviruses. Anchor and dimerization, but not glycosylation of GPI (show GPI Proteins)-Linked Membrane Proteins are essential for antiviral activity of bBST2A1.
the detected relationship between BST2 expression and viral load as well as with MX1 (show MX1 Proteins) indicate a common regulation by the interferon (show IFNA Proteins) response and suggest rather limited influence of BST2 in vivo on the simian immunodeficiency virus infection outcome
Data suggest that rhesus macaque tetherin and Simian immunodeficiency virus Nef undergo physical interaction leading to removal of tetherin from plasma membrane by clathrin-mediated endocytosis.
A 5-amino-acid sequence in the rhesus BST-2 cytoplasmic domain accounts for the interaction with Vpu and for rhesus BST-2 antagonism by HIV-1 Vpu.
Simian immunodeficiency virus infection results in rapid upregulation of BST-2 on peripheral blood lymphocytes.
Indirect immunofluorescence assay and western blot analysis showed that the MAb was specifically reacted with the overexpressed porcine BST-2 protein in Vero cells. The specific MAb of porcine BST-2 provides a valuable tool for further studies of BST-2 to restrict virus infection
This antibody only reacted with porcine BST-2 protein and not with human, monkey, or mouse BST-2 protein
PRRSV counteract the antiviral functions of IFITM1 (show IFITM1 Proteins) and Tetherin by the interaction of the Nsp3 (show SH2D3C Proteins) with IFITM1 (show IFITM1 Proteins) and the E protein with Tetherin.
The BST2 had antiviral activity against vesicular stomatitis virus, avian influenza virus and Porcine reproductive and respiratory syndrome virus.
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 (show NFKB1 Proteins) signaling.
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.
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.
BST2 likely mediates platinum resistance in nasopharyngeal cancer via NF-kappaB (show NFKB1 Proteins) signaling
These data collectively suggest that the human parainfluenza virus type 2 V protein inhibits tetherin expression induced by several external stimuli.
These results suggest that tetherin antagonism by V proteins is common among the genus Rubulavirus.
High BST2 expression is associated with Esophageal, Gastric, or Colorectal Cancer.
Two additional regulators of BST2 constitutive ubiquitylation and sorting to the lysosomes: the E3 ubiquitin ligases NEDD4 and MARCH8, are reported.
Coimmunoprecipitation studies indicated that non-glycosylated tetherin is stabilized through the formation of a ternary SGTA (show SGTA Proteins)/Vpu/tetherin complex. Although the results do not provide support for a physiological function of SGTA (show SGTA Proteins) in HIV-1 replication, they demonstrate that SGTA (show SGTA Proteins) overexpression regulates tetherin expression and stability, thus providing insights into the function of SGTA (show SGTA Proteins) in endoplasmic reticulum translocation
Importantly, the authors demonstrate for the first time that the HIV-2 Env (show ERVW-1 Proteins) induces NF-kappaB (show NFKB1 Proteins) activation in HEKappa293T cells. Furthermore, the anti-BST-2 activity of the HIV-2 Env (show ERVW-1 Proteins) is not sufficient to completely inhibit NF-kappaB (show NFKB1 Proteins) activity.
contain the spread of herpes simplex virus type 1 in vivo, STING-dependent signaling leads to the upregulation of tetherin, a viral restriction factor
Tetherin-mediated retention of R-defective virions on the cell surface could enhance syncytium formation.
Bone marrow stromal antigen 2-mediated dendritic cell activation as a critical mechanism for how Tetherin influenced retrovirus cell-mediated immune responses that subsequently inhibited retrovirus replication in vivo.
BST-2 does not have a role in modulating Influenza A Virus in the mouse model of infection
Although Bst2 prevented Measles virus (MV) release from nonneuronal cells, its deletion had no effect on viral pathogenesis in MV-challenged mice.
BST-2 contributes to the emergence of neoplasia and malignant progression of breast cancer. BST-2 enhances cancer cell adhesion, anchorage-independency, migration, and invasion.
BST-2 protects lymphoid tissues from Chikungunya virus (CHIKV) infection and regulates CHIKV-induced inflammatory response by the host.
TLR4 (show TLR4 Proteins) and PI3K effects on BST-2 induction are at the level of transcription.
Tetherin acts as a modulator of the cell-mediated immune response against retrovirus infection in vivo.
These findings suggest that BST2 antagonism by Vpu is critical for efficient early viral expansion and dissemination during acute infection and as such is likely to confer HIV-1 increased transmission fitness.
Bone marrow stromal cells are involved in the growth and development of B-cells. The specific function of the protein encoded by the bone marrow stromal cell antigen 2 is undetermined\; however, this protein may play a role in pre-B-cell growth and in rheumatoid arthritis.
bone marrow stromal antigen 2
, bone marrow stromal cell antigen 2
, HM1.24 antigen
, DAMP-1 protein homolog
, protein DAMP-1