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Data suggest that both HVEM and UL144 bind a common epitope of BTLA, whether engaged in trans or in cis; these studies were conducted in cell lines representing B-lymphocytes, T-lymphocytes, and natural killer cells. (HVEM = human herpes virus entry mediator; UL144 = membrane glycoprotein UL144 of Human herpesvirus 5; BTLA = human B- and T-lymphocyte attenuator)
our data suggested that the BTLA/HVEM pathway contributes to peripheral T cell suppression in hepatocellular carcinoma patients
TNFRSF14 may serve a tumor suppressive role in bladder cancer by inducing apoptosis and suppressing proliferation, and act as a novel prognostic biomarker for bladder cancer.
Primary cutaneous follicle center lymphomas with concomitant 1p36 deletion and TNFRSF14 mutations frequently express high levels of EZH2 protein.
High HVEM Expression is Associated with Cancer Progression in Breast Cancer.
Report a variant of t(14;18) negative nodal diffuse follicular lymphoma with CD23 expression, 1p36/TNFRSF14 abnormalities, and STAT6 mutations.
Roles of HVEM are likely to be immunosuppressive rather than activating tumor immunity and it in peripheral blood is a diagnostic marker and therapeutic target for hepatocellular carcinoma.
Low HVEM expression is associated with pancreatic and ampullary cancer.
HIV-1 produced from CD4+ T cells bears HSV-2 receptor HVEM and can bind to and enter HSV-2-infected epithelial cells depending on HVEM-gD interaction and the presence of gB/gH/gL.
Transgenic mice expressing HVEMIg showed a complete resistance to the lethal infection even with 300 MLD50 (survival rate of 100 %).
HVEM is highly expressed in ovarian serous adenocarcinoma tissues and correlated with the patient clinicopathological features.
TNFRSF14 and MAP2K1 mutations are the most frequent genetic alterations found in pediatric-type follicular lymphoma (PTFL) and occur independently in most cases, suggesting that both mutations might play an important role in PTFL lymphomagenesis.
genetic landscape of Pediatric-type follicular lymphoma suggests that TNFRSF14 mutations accompanied by copy-number neutral loss of heterozygosity of the 1p36 locus in over 70% of mutated cases, as additional selection mechanism, might play a key role in the pathogenesis of this disease.
The increased immune-stimulatory capacity of lymphoma B cells with TNFRSF14 aberrations had clinical relevance, associating with higher incidence of acute GVHD in patients undergoing allogeneic hematopoietic stem cell transplantation.
These results suggest that TNFRSF14 mutations point towards a diagnosis of follicular lymphomas , and can be used in the sometimes difficult distinction between marginal zone lymphomas and follicular lymphomas
the overexpression of HVEM in ovarian cancer cells may suppress the proliferation and immune function of T cells, thus leading to the development of ovarian cancer. The current study partially explains the immune escape mechanism of ovarian cancer cells.
In eight cases (42%) we observed recurrent copy number loss of chr1:2,352,236-4,574,271, a region containing the candidate tumor suppressor TNFRSF14.
Study report the crystal structure of unbound HVEM, which further contributes to the understanding of the molecular mechanisms controlling recognition between HVEM and its ligands.
HVEM may play a critical role in tumor progression and immune evasion
Data indicate that tumour-expressing herpes virus entry mediator (HVEMplays a critical role in hepatocellular carcinoma (HCC), suggesting targeting HVEM may be a promising therapeutic strategy for HCC.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor was identified as a cellular mediator of herpes simplex virus (HSV) entry. Binding of HSV viral envelope glycoprotein D (gD) to this receptor protein has been shown to be part of the viral entry mechanism. The cytoplasmic region of this receptor was found to bind to several TRAF family members, which may mediate the signal transduction pathways that activate the immune response.
tumor necrosis factor receptor superfamily member 14
, tumor necrosis factor receptor superfamily, member 14 (herpesvirus entry mediator)
, herpesvirus entry mediator A
, CD40-like protein
, herpes virus entry mediator A
, tumor necrosis factor receptor-like 2
, tumor necrosis factor receptor-like gene2
, herpes virus entry mediator