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anti-Human TNFRSF14 Antikörper:
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Human Monoclonal TNFRSF14 Primary Antibody für FACS - ABIN4897515
Wang, Wen, Routy, Bernard, Sekaly, Watts et al.: 4-1BBL induces TNF receptor-associated factor 1-dependent Bim modulation in human T cells and is a critical component in the costimulation-dependent rescue of functionally impaired HIV-specific CD8 T ... in Journal of immunology (Baltimore, Md. : 1950) 2007
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Human Monoclonal TNFRSF14 Primary Antibody für CyTOF, ELISA (Capture) - ABIN4900305
Kang, Kim, Kang, Han, Nam, Kyung, Park, Kim: LIGHT up-regulated on B lymphocytes and monocytes in rheumatoid arthritis mediates cellular adhesion and metalloproteinase production by synoviocytes. in Arthritis and rheumatism 2007
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Human Polyclonal TNFRSF14 Primary Antibody für WB - ABIN550239
Granger, Rickert: LIGHT-HVEM signaling and the regulation of T cell-mediated immunity. in Cytokine & growth factor reviews 2003
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Human Polyclonal TNFRSF14 Primary Antibody für WB - ABIN550240
Watts: TNF/TNFR family members in costimulation of T cell responses. in Annual review of immunology 2005
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Human Monoclonal TNFRSF14 Primary Antibody für FACS, ELISA - ABIN610276
Ohmstede, Bland, Merrill, Sahyoun: Relationship of genes encoding Ca2+/calmodulin-dependent protein kinase Gr and calspermin: a gene within a gene. in Proceedings of the National Academy of Sciences of the United States of America 1991
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Human Polyclonal TNFRSF14 Primary Antibody für ELISA, WB - ABIN547562
Cheung, Humphreys, Potter, Norris, Shumway, Tran, Patterson, Jean-Jacques, Yoon, Spear, Murphy, Lurain, Benedict, Ware: Evolutionarily divergent herpesviruses modulate T cell activation by targeting the herpesvirus entry mediator cosignaling pathway. in Proceedings of the National Academy of Sciences of the United States of America 2005
Human Polyclonal TNFRSF14 Primary Antibody für ICC, ELISA - ABIN1002432
Marsters, Ayres, Skubatch, Gray, Rothe, Ashkenazi et al.: Herpesvirus entry mediator, a member of the tumor necrosis factor receptor (TNFR) family, interacts with members of the TNFR-associated factor family and activates the transcription factors NF-kappaB ... in The Journal of biological chemistry 1997
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Human Polyclonal TNFRSF14 Primary Antibody für ELISA, ICC - ABIN4320720
Abadpour, Halvorsen, Sahraoui, Korsgren, Aukrust, Scholz: Interleukin-22 reverses human islet dysfunction and apoptosis triggered by hyperglycemia and LIGHT. in Journal of molecular endocrinology 2018
the BTLA-TNFRSF14 immune modulation pathway seems to play a role in the pathobiology and prognosis of FL.
LIGHT signaling through HVEM in epidermal keratinocytes directly induced proliferation and periostin expression, and both keratinocyte-specific deletion of HVEM or antibody blocking of LIGHT-HVEM interactions after disease onset prevented expression of periostin and limited atopic dermatitis symptoms.
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.
Mice with a conditional deletion of the LIGHT receptor HVEM (herpesvirus entry mediator) in keratinocytes phenocopied LIGHT-deficient mice in exhibiting reduced epidermal thickening and dermal collagen deposition in a model of atopic dermatitis driven by house dust mite allergen.
these data indicate that HVEM/BTLA interactions are dispensable for the formation of de novo host antidonor isotype-specific antibodies following skin transplantation
LIGHT promote myeloid differentiation of Hematopoietic stem/progenitor cells via LIGHT receptor signaling.
HVEM represents a critical signal for memory precursor effector cells and development of protective mucosal CD8 T cell memory
Dendritic cells require BTLA and HVEM to actively adjust tolerizing T cell responses under steady-state conditions.
we identified herpes virus entry mediator as a functional receptor that mediates SALM5's suppressive function. Our findings reveal a molecular link between the neuronal system and the immune system, and provide potential therapeutic targets for the control of CNS diseases.
results have revealed a novel role of HVEM on the regulation of IFN-I and immunopathology during Listeria infection.
our studies revealed a novel function of the HVEM cosignaling molecule and its ligands in EAU pathogenesis through the induction of Th1- and Th17-type T cell responses
Together, these data indicate that HVEM contributes to ocular pathogenesis independently of entry and point to an immunomodulatory role for this protein specifically on radiation-resistant cells.
results demonstrate a role for both nectin-1 and HVEM as receptors and suggest a further receptor which appears much less efficient.
Authors show that CD4(+) FoxP3(+) Tregs up- regulate HVEM (herpes virus entry mediator), which is a binding site for major viral glycoprotein gD, following herpes simplex virus 1 infection.
results support a model whereby BTLA on innate leukocytes is triggered by HVEM and delivers negative signals into BTLA(+) cells, thereby interfering with the protective immune response to this intestinal parasite.
In summary, herpes simplex virus 1 entry into epidermis was shown to strongly depend on the presence of nectin-1, but the restricted presence of HVEM can potentially replace nectin-1 as a receptor.
One mechanism by which the herpes simplex virus 1 latency-associated transcript enhances latency and reactivation appears to be by upregulating HVEM expression.
Data indicate taht tumor necrosis factor receptor superfamily member 14 (TNFRSF14)participated in ovariectomy (OVX)-induced adipose tissue (AT) inflammation via upregulation of CD11c, resulting in metabolic perturbation.
These results suggest that differences in nectin-1 and HVEM receptor expression between adults and newborns may partially explain differences in susceptibility to herpes simplex 2.
uncover a unique role for HVEM in mediating HSV-1 infection in an area innervated by the trigeminal ganglion and may explain why the presence of HVEM can lead to severe inflammation in the cornea
Our findings indicate that HVEM regulates bone remodeling via action on osteoclasts.
These findings support role for BTLA and/or HVEM as potential, novel diagnostic markers of innate immune response/status and as therapeutic targets of sepsis.
results pinpoint HVEM as an important orchestrator of mucosal immunity, integrating signals from innate lymphocytes to induce optimal epithelial Stat3 activation, which indicates that targeting HVEM with agonists could improve host defence
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