Receptors, Tumor Necrosis Factor, Member 14
"Receptors, Tumor Necrosis Factor, Member 14" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A novel member of the tumor-necrosis factor receptor family that can also mediate HERPES SIMPLEX VIRUS TYPE 1 entry into cells. It has specificity for TUMOR NECROSIS FACTOR LIGAND SUPERFAMILY MEMBER 14 and the homotrimeric form of LYMPHOTOXIN-ALPHA. The receptor is abundantly expressed on T-LYMPHOCYTES and may play a role in regulating lymphocyte activation. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
| Descriptor ID |
D053240
|
| MeSH Number(s) |
D12.776.543.750.705.852.760.500 D12.776.543.750.830.850
|
| Concept/Terms |
Receptors, Tumor Necrosis Factor, Member 14- Receptors, Tumor Necrosis Factor, Member 14
- HveA Protein
- Tumor Necrosis Factor Receptor Superfamily, Member 14
- Tumor Necrosis Factor Receptor Subfamily, Member 14
- HVEM Protein
- Herpesvirus Entry Mediator
- Entry Mediator, Herpesvirus
|
Below are MeSH descriptors whose meaning is more general than "Receptors, Tumor Necrosis Factor, Member 14".
- Chemicals and Drugs [D]
- Amino Acids, Peptides, and Proteins [D12]
- Proteins [D12.776]
- Membrane Proteins [D12.776.543]
- Receptors, Cell Surface [D12.776.543.750]
- Receptors, Immunologic [D12.776.543.750.705]
- Receptors, Cytokine [D12.776.543.750.705.852]
- Receptors, Tumor Necrosis Factor [D12.776.543.750.705.852.760]
- Receptors, Tumor Necrosis Factor, Member 14 [D12.776.543.750.705.852.760.500]
- Receptors, Virus [D12.776.543.750.830]
- Receptors, Tumor Necrosis Factor, Member 14 [D12.776.543.750.830.850]
Below are MeSH descriptors whose meaning is more specific than "Receptors, Tumor Necrosis Factor, Member 14".
This graph shows the total number of publications written about "Receptors, Tumor Necrosis Factor, Member 14" by people in this website by year, and whether "Receptors, Tumor Necrosis Factor, Member 14" was a major or minor topic of these publications.
View timeline visualization
| Year | Major Topic | Minor Topic | Total |
|---|
| 1997 | 0 | 1 | 1 |
| 2002 | 0 | 1 | 1 |
| 2005 | 0 | 1 | 1 |
| 2006 | 1 | 1 | 2 |
| 2009 | 1 | 0 | 1 |
| 2011 | 1 | 0 | 1 |
| 2012 | 0 | 1 | 1 |
| 2016 | 1 | 1 | 2 |
| 2018 | 0 | 1 | 1 |
| 2019 | 1 | 0 | 1 |
| 2020 | 0 | 1 | 1 |
| 2022 | 1 | 0 | 1 |
Below are the most recent publications written about "Receptors, Tumor Necrosis Factor, Member 14" by people in Profiles.
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Lymphotoxin beta receptor signaling directly controls airway smooth muscle deregulation and asthmatic lung dysfunction. J Allergy Clin Immunol. 2023 04; 151(4):976-990.e5.
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Increased Production of LIGHT by T Cells in Eosinophilic Esophagitis Promotes Differentiation of Esophageal Fibroblasts Toward an Inflammatory Phenotype. Gastroenterology. 2020 11; 159(5):1778-1792.e13.
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Indolent In Situ B-Cell Neoplasms With MYC Rearrangements Show Somatic Mutations in MYC and TNFRSF14 by Next-generation Sequencing. Am J Surg Pathol. 2019 12; 43(12):1720-1725.
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The HVEM-BTLA Axis Restrains T Cell Help to Germinal Center B Cells and Functions as a Cell-Extrinsic Suppressor in Lymphomagenesis. Immunity. 2019 08 20; 51(2):310-323.e7.
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Herpes Simplex Virus 1 Latency and the Kinetics of Reactivation Are Regulated by a Complex Network of Interactions between the Herpesvirus Entry Mediator, Its Ligands (gD, BTLA, LIGHT, and CD160), and the Latency-Associated Transcript. J Virol. 2018 12 15; 92(24).
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LIGHT-HVEM Signaling in Innate Lymphoid Cell Subsets Protects Against Enteric Bacterial Infection. Cell Host Microbe. 2018 08 08; 24(2):249-260.e4.
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Rubinstein-Taybi syndrome - a window into follicular lymphoma biology. Leuk Lymphoma. 2016 12; 57(12):2908-2910.
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Characterization of a variant of t(14;18) negative nodal diffuse follicular lymphoma with CD23 expression, 1p36/TNFRSF14 abnormalities, and STAT6 mutations. Mod Pathol. 2016 06; 29(6):570-81.
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BTLA interaction with HVEM expressed on CD8(+) T cells promotes survival and memory generation in response to a bacterial infection. PLoS One. 2013; 8(10):e77992.
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A herpes simplex virus 2 glycoprotein D mutant generated by bacterial artificial chromosome mutagenesis is severely impaired for infecting neuronal cells and infects only Vero cells expressing exogenous HVEM. J Virol. 2012 Dec; 86(23):12891-902.