"Transcription Factors" 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.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
| Descriptor ID |
D014157
|
| MeSH Number(s) |
D12.776.930
|
| Concept/Terms |
Transcription Factors- Transcription Factors
- Factors, Transcription
- Transcription Factor
- Factor, Transcription
|
Below are MeSH descriptors whose meaning is more general than "Transcription Factors".
Below are MeSH descriptors whose meaning is more specific than "Transcription Factors".
This graph shows the total number of publications written about "Transcription Factors" by people in this website by year, and whether "Transcription Factors" was a major or minor topic of these publications.
To see the data from this visualization as text,
click here.
| Year | Major Topic | Minor Topic | Total |
|---|
| 1994 | 45 | 17 | 62 |
| 1995 | 37 | 14 | 51 |
| 1996 | 57 | 20 | 77 |
| 1997 | 56 | 36 | 92 |
| 1998 | 73 | 24 | 97 |
| 1999 | 84 | 35 | 119 |
| 2000 | 100 | 42 | 142 |
| 2001 | 103 | 36 | 139 |
| 2002 | 95 | 52 | 147 |
| 2003 | 98 | 60 | 158 |
| 2004 | 116 | 69 | 185 |
| 2005 | 92 | 80 | 172 |
| 2006 | 54 | 52 | 106 |
| 2007 | 73 | 51 | 124 |
| 2008 | 55 | 40 | 95 |
| 2009 | 60 | 51 | 111 |
| 2010 | 68 | 52 | 120 |
| 2011 | 65 | 53 | 118 |
| 2012 | 74 | 50 | 124 |
| 2013 | 72 | 64 | 136 |
| 2014 | 54 | 70 | 124 |
| 2015 | 66 | 50 | 116 |
| 2016 | 57 | 50 | 107 |
| 2017 | 43 | 40 | 83 |
| 2018 | 46 | 26 | 72 |
| 2019 | 38 | 42 | 80 |
| 2020 | 45 | 41 | 86 |
| 2021 | 33 | 33 | 66 |
| 2022 | 18 | 48 | 66 |
| 2023 | 21 | 56 | 77 |
| 2024 | 21 | 33 | 54 |
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Below are the most recent publications written about "Transcription Factors" by people in Profiles.
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Evidence that CRISPR-Cas9 Y537S-mutant expressing breast cancer cells activate Yes-associated protein 1 to driving the conversion of normal fibroblasts into cancer-associated fibroblasts. Cell Commun Signal. 2024 Nov 14; 22(1):545.
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STEMIN and YAP5SA, the future of heart repair? Exp Biol Med (Maywood). 2024; 249:10246.
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Pathogenic SATB2 missense variants affecting p.Gly392 have variable functional implications and result in diverse clinical phenotypes. J Med Genet. 2024 Oct 23; 61(11):1062-1067.
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Sall4 and Gata4 induce cardiac fibroblast transition towards a partially multipotent state with cardiogenic potential. Sci Rep. 2024 10 15; 14(1):24182.
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YAP1 Status Defines Two Intrinsic Subtypes of LCNEC with Distinct Molecular Features and Therapeutic Vulnerabilities. Clin Cancer Res. 2024 Oct 15; 30(20):4743-4754.
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Molecular architecture and functional dynamics of the pre-incision complex in nucleotide excision repair. Nat Commun. 2024 Oct 01; 15(1):8511.
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Exploration of the tunability of BRD4 degradation by DCAF16 trans-labelling covalent glues. Eur J Med Chem. 2024 Dec 05; 279:116904.
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Non-coding cause of congenital heart defects: Abnormal RNA splicing with multiple isoforms as a mechanism for heterotaxy. HGG Adv. 2024 Oct 10; 5(4):100353.
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Prognostic Impact of Notch1 Intracellular Domain, P63, and c-MYC in Lacrimal Gland Adenoid Cystic Carcinoma. Invest Ophthalmol Vis Sci. 2024 Sep 03; 65(11):4.
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A PRDM16-driven signal regulates body composition in testosterone-treated hypogonadal men. Front Endocrinol (Lausanne). 2024; 15:1426175.