Transcription Factor RelA
"Transcription Factor RelA" 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 subunit of NF-kappa B that is primarily responsible for its transactivation function. It contains a C-terminal transactivation domain and an N-terminal domain with homology to PROTO-ONCOGENE PROTEINS C-REL.
| Descriptor ID |
D051996
|
| MeSH Number(s) |
D12.776.260.600.249 D12.776.660.600.249 D12.776.930.600.249
|
| Concept/Terms |
Transcription Factor RelA- Transcription Factor RelA
- RelA, Transcription Factor
- NF-kappa B p65
- NF kappa B p65
- p65, NF-kappa B
- NF-kappa B p65 Subunit
- NF kappa B p65 Subunit
- Transcription Factor p65
- p65, Transcription Factor
- p65 Transcription Factor
- Transcription Factor, p65
- v-Rel Reticuloendotheliosis Viral Oncogene Homolog A
- v Rel Reticuloendotheliosis Viral Oncogene Homolog A
- NF-kappaB 65-kDa
- NF kappaB 65 kDa
|
Below are MeSH descriptors whose meaning is more general than "Transcription Factor RelA".
Below are MeSH descriptors whose meaning is more specific than "Transcription Factor RelA".
This graph shows the total number of publications written about "Transcription Factor RelA" by people in this website by year, and whether "Transcription Factor RelA" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 1999 | 0 | 1 | 1 |
| 2000 | 0 | 3 | 3 |
| 2003 | 0 | 1 | 1 |
| 2004 | 0 | 2 | 2 |
| 2005 | 0 | 2 | 2 |
| 2006 | 1 | 0 | 1 |
| 2007 | 2 | 3 | 5 |
| 2008 | 0 | 2 | 2 |
| 2009 | 3 | 0 | 3 |
| 2010 | 2 | 1 | 3 |
| 2011 | 2 | 2 | 4 |
| 2012 | 1 | 1 | 2 |
| 2013 | 1 | 1 | 2 |
| 2014 | 1 | 1 | 2 |
| 2017 | 1 | 1 | 2 |
| 2019 | 1 | 1 | 2 |
| 2020 | 1 | 1 | 2 |
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Below are the most recent publications written about "Transcription Factor RelA" by people in Profiles.
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A Hyperactive RelA/p65-Hexokinase 2 Signaling Axis Drives Primary Central Nervous System Lymphoma. Cancer Res. 2020 12 01; 80(23):5330-5343.
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FSTL-1 Attenuation Causes Spontaneous Smoke-Resistant Pulmonary Emphysema. Am J Respir Crit Care Med. 2020 04 15; 201(8):934-945.
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Causative role of PDLIM2 epigenetic repression in lung cancer and therapeutic resistance. Nat Commun. 2019 11 22; 10(1):5324.
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Optical Pooled Screens in Human Cells. Cell. 2019 10 17; 179(3):787-799.e17.
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NLRX1 modulates differentially NLRP3 inflammasome activation and NF-?B signaling during Fusobacterium nucleatum infection. Microbes Infect. 2018 Oct - Nov; 20(9-10):615-625.
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IL-18 Drives ILC3 Proliferation and Promotes IL-22 Production via NF-?B. J Immunol. 2017 10 01; 199(7):2333-2342.
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C11orf95-RELA fusion present in a primary supratentorial ependymoma and recurrent sarcoma. Brain Tumor Pathol. 2015 Apr; 32(2):105-11.
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Fli-1 controls transcription from the MCP-1 gene promoter, which may provide a novel mechanism for chemokine and cytokine activation. Mol Immunol. 2015 Feb; 63(2):566-73.
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Reining in nuclear factor-kappaB in skeletal muscle disorders. Curr Opin Clin Nutr Metab Care. 2013 May; 16(3):251-7.
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Transcriptional regulation of increased CCL2 expression in pulmonary fibrosis involves nuclear factor-?B and activator protein-1. Int J Biochem Cell Biol. 2013 Jul; 45(7):1366-76.