Results 91 to 100 of about 6,331 (185)

Multiple surfaces of BST2 are required for Spike-mediated antagonism.

open access: yes
Extended data for Fig 5. (A) Diagram of the architecture of BST2 and BST2 mutants. CT: cytoplasmic tail. TM: transmembrane domain. EC1: extracellular domain region 1. CC: coiled-coil domain. EC2: extracellular domain region 2.
Sydney Simpson (5132285)   +5 more
core   +1 more source

HCMV induces BST2 independent of IFN, but inhibits IFN-dependent induction.

open access: yes, 2013
A) Expression of BST2 monitored by flow cytometry using anti-BST2 (HM1.24) antibody is shown in all panels except for the shaded graph in the top left panel that shows staining of secondary antibody alone.
Mandana Mansouri (340371)   +5 more
core   +1 more source

Comprehensive Antiretroviral Restriction Factor Profiling Reveals the Evolutionary Imprint of the ex Vivo and in Vivo IFN-β Response in HTLV-1-Associated Neuroinflammation

open access: yesFrontiers in Microbiology, 2018
HTLV-1-Associated Myelopathy (HAM/TSP) is a progressive neuroinflammatory disorder for which no disease-modifying treatment exists. Modest clinical benefit from type I interferons (IFN-α/β) in HAM/TSP contrasts with its recently identified IFN-inducible ...
Fabio E. Leal   +15 more
doaj   +1 more source

LC3C Contributes to Vpu-Mediated Antagonism of BST2/Tetherin Restriction on HIV-1 Release through a Non-canonical Autophagy Pathway [PDF]

open access: yes, 2016
SummaryBST2 (bone marrow stromal antigen 2)/tetherin is a restriction factor of enveloped viruses, which blocks the release of viral particles. HIV-1 encodes proteins that antagonize this innate barrier, including the accessory protein Vpu.
Frémont, Stéphane   +7 more
core   +1 more source

Mechanisms underlying HIV-1 Vpu-mediated viral egress

open access: yesFrontiers in Microbiology, 2014
Viruses such as lentiviruses that are responsible for long lasting infections, have to evade several level of cellular immune mechanisms to persist and efficiently disseminate in the host.
Nicolas eRoy   +3 more
doaj   +1 more source

The degree of BST2 expression in A549-ACE2-BST2 cells is comparable to that afforded by IFNα stimulation.

open access: yes
The levels of BST2 in A549-ACE2 cells engineered to constitutively express BST2 were compared to HeLa cells, which express BST2 endogenously, and parental A549-ACE2 cells treated with IFNα.
Sydney Simpson (5132285)   +5 more
core   +1 more source

BST2/Tetherin enhances HCMV infection and release.

open access: yes, 2013
A) A schematic representation of the BST2 constructs used in this study. B) Immunoblot for HCMV-IE1 or GAPDH of HFFs exposed to supernatants of HCMV-infected THFs expressing BST2-HA146 or vector control.
Mandana Mansouri (340371)   +5 more
core   +1 more source

DYSREGULATION OF THE ILT7/BST2 PDC NEGATIVE FEEDBACK BY HIV-1:IMPLICATIONS FOR HIV-1 TRANSMISSION AND IMMUNOPATHOGENESIS [PDF]

open access: yes, 2013
Introduction: The immunoglobulin like transcript 7 (ILT7) is a surface molecule selectively expressed by human plasmacytoid dendritic cell (pDC). ILT7 cross-linking inhibits Toll like receptor (TLR) 7/9-mediated pDC activation and type I interferon (IFNI)
TAVANO, BARBARA
core   +1 more source

Increased BST2 expression during simian immunodeficiency virus infection is not a determinant of disease progression in rhesus monkeys [PDF]

open access: yes, 2015
BACKGROUND: Bone marrow stromal cell antigen 2 (BST2), also known as tetherin, HM1.24 or CD317 represents a type 2 integral membrane protein, which has been described to restrict the production of some enveloped viruses by inhibiting the virus release ...
Katharina Töpfer (319929)   +9 more
core   +1 more source

Le facteur de restriction viral BST2/Tetherin ancre les Midbody post-cytokinétiques à la surface cellulaire

open access: yes, 2020
The Midbody Remnant (MBR) is a structure that arises once cytokinetic abscission, the last step in cell division, is completed. Then, the MBR interacts with the cell surface and can play various roles in development, polarisation or cell proliferation. I
Presle, Adrien
core   +1 more source

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