Receptors, Tumor Necrosis Factor, Type I
"Receptors, Tumor Necrosis Factor, Type I" 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 tumor necrosis factor receptor subtype that has specificity for TUMOR NECROSIS FACTOR ALPHA and LYMPHOTOXIN ALPHA. It is constitutively expressed in most tissues and is a key mediator of tumor necrosis factor signaling in the vast majority of cells. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
| Descriptor ID |
D047888
|
| MeSH Number(s) |
D12.776.543.750.690.750 D12.776.543.750.705.852.760.597
|
| Concept/Terms |
Receptors, Tumor Necrosis Factor, Type I- Receptors, Tumor Necrosis Factor, Type I
- Receptors, Tumor Necrosis Factor, Member 1A
- TNFR p60
- TNFR-I
- Tumor Necrosis Factor Receptor Type I
- TNFR1
- Tumor Necrosis Factor Receptor 1A
- TNFRSF1A (Tumor Necrosis Factor Receptor Superfamily, Member 1A)
- Tumor Necrosis Factor Receptor Type 1
- Antigens, CD120a
- CD120a Antigens
- TNFRSF1A Receptor
- Receptor, TNFRSF1A
- Tumor Necrosis Factor Receptor Superfamily, Member 1A
- CD 120a Antigen
- 120a Antigen, CD
- Antigen, CD 120a
- CD120a Antigen
- Antigen, CD120a
|
Below are MeSH descriptors whose meaning is more general than "Receptors, Tumor Necrosis Factor, Type I".
- 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, Death Domain [D12.776.543.750.690]
- Receptors, Tumor Necrosis Factor, Type I [D12.776.543.750.690.750]
- 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, Type I [D12.776.543.750.705.852.760.597]
Below are MeSH descriptors whose meaning is more specific than "Receptors, Tumor Necrosis Factor, Type I".
This graph shows the total number of publications written about "Receptors, Tumor Necrosis Factor, Type I" by people in this website by year, and whether "Receptors, Tumor Necrosis Factor, Type I" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 1998 | 0 | 1 | 1 |
| 2003 | 0 | 1 | 1 |
| 2004 | 0 | 1 | 1 |
| 2006 | 1 | 0 | 1 |
| 2008 | 1 | 0 | 1 |
| 2010 | 1 | 0 | 1 |
| 2013 | 1 | 1 | 2 |
| 2014 | 1 | 0 | 1 |
| 2017 | 0 | 2 | 2 |
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Below are the most recent publications written about "Receptors, Tumor Necrosis Factor, Type I" by people in Profiles.
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Association Between Inflammatory Markers and Progression to Kidney Dysfunction: Examining Different Assessment Windows in Patients With Type 1 Diabetes. Diabetes Care. 2018 01; 41(1):128-135.
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Immune complexes containing malondialdehyde (MDA) LDL induce apoptosis in human macrophages. Clin Immunol. 2018 02; 187:1-9.
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Response to comment on Lopes-Virella et al. Baseline markers of inflammation are associated with progression to macroalbuminuria in type 1 diabetic subjects. Diabetes care 2013;36:2317-2323. Diabetes Care. 2014 May; 37(5):e108-9.
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Inhibitor ?B kinase 2 is a myosin light chain kinase in vascular smooth muscle. Circ Res. 2013 Aug 16; 113(5):562-70.
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Baseline markers of inflammation are associated with progression to macroalbuminuria in type 1 diabetic subjects. Diabetes Care. 2013 Aug; 36(8):2317-23.
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TNFR1 delivers pro-survival signals that are required for limiting TNFR2-dependent activation-induced cell death (AICD) in CD8+ T cells. Eur J Immunol. 2011 Feb; 41(2):335-44.
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Aprotinin exacerbates left ventricular dysfunction after ischemia/reperfusion in mice lacking tumor necrosis factor receptor I. J Cardiovasc Pharmacol. 2008 Oct; 52(4):355-62.
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Graft tumor necrosis factor receptor-1 protects after mouse liver transplantation whereas host tumor necrosis factor receptor-1 promotes injury. Transplantation. 2006 Nov 15; 82(9):1214-20.
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Differential requirement for c-Jun NH2-terminal kinase in TNFalpha- and Fas-mediated apoptosis in hepatocytes. FASEB J. 2004 Apr; 18(6):720-2.
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Bid activates multiple mitochondrial apoptotic mechanisms in primary hepatocytes after death receptor engagement. Gastroenterology. 2003 Sep; 125(3):854-67.