Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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-Linked Membrane Proteins are essential for antiviral activity of bBST2A1.
the detected relationship between BST2 expression and viral load as well as with MX1 indicate a common regulation by the interferon 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 and Tetherin by the interaction of the Nsp3 with IFITM1 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.
BST2 recruits the E3 ubiquitin ligase MARCH8 to catalyze the K27-linked ubiquitination of MAVS for CALCOCO2-directed autophagic degradation.
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.
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.
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 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/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
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.
Data revealed that under a nutrient deficient condition, CD317 functions as an anti-apoptotic factor through AIF-mediated caspase and autophagy-independent manner.
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
a non-canonical autophagy pathway reminiscent of LC3-associated phagocytosis contributes to Vpu counteraction of BST2 restriction.
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.
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.
Disruption of BST-2 dimerization offers a potential therapeutic approach for breast cancer.
identified WDR81 as a novel gene required for tetherin trafficking and degradation in both the presence and absence of Vpu
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.
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 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.
These data suggest that overexpression of BST-2 in carcinoma tissues could not be attributed to interferons but to a yet to be determined factor that upregulates BST-2 once oncogenesis is initiated.
Taken together, our results indicate that BST-2 is an important factor in the invasiveness and motility of tamoxifen-resistant breast cancer cells, and that its expression and activity are regulated by activated STAT3.
BST-2 is a useful receptor to target with antigen, given its broad expression pattern and ability to access both MHCI and MHCII presentation pathways with relative efficiency.
A single nucleotide polymorphism in tetherin promotes retrovirus restriction in vivo.
find that tetherin markedly inhibits the replication of Moloney murine leukemia virus (Mo-MLV) and is required for the antiretroviral activity of IFNalpha to be fully manifested in vitro.
These data provide evidence that BST-2 restricts mouse mammary tumor virus release from naturally infected cells and that BST-2 is an antiviral factor in vivo.
These findings reflect involvement of BST2 in endocytosis and intracellular trafficking of viruses, viral nucleic acids, and Ags.
Tetherin is expressed on the plasma membrane outer face of neuroblastoma cells, can be induced with both IFN-gamma & IFN-beta, & restricts progeny VSV release up to 100-fold, contributing to a potent antiviral state in the host cell.
BST2-mediated Ag delivery in the presence of polyinosinic-polycytidylic acid as adjuvant induces cytotoxic T lymphocytes that are functional in vivo
Structural and biophysical analysis of BST-2/tetherin ectodomains reveals an evolutionary conserved design to inhibit virus release.
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