"Smad Proteins" 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 family of proteins that are involved in the translocation of signals from TGF-BETA RECEPTORS; BONE MORPHOGENETIC PROTEIN RECEPTORS; and other surface receptors to the CELL NUCLEUS. They were originally identified as a class of proteins that are related to the mothers against decapentaplegic protein, Drosophila and sma proteins from CAENORHABDITIS ELEGANS.
| Descriptor ID |
D051785
|
| MeSH Number(s) |
D12.644.360.024.334 D12.776.157.057.170 D12.776.260.713 D12.776.476.024.428 D12.776.930.806
|
| Concept/Terms |
Smad Proteins- Smad Proteins
- Mothers Against Decapentaplegic Homolog
- Sma- and Mad-Related Proteins
|
Below are MeSH descriptors whose meaning is more general than "Smad Proteins".
Below are MeSH descriptors whose meaning is more specific than "Smad Proteins".
This graph shows the total number of publications written about "Smad Proteins" by people in this website by year, and whether "Smad Proteins" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 2004 | 0 | 1 | 1 |
| 2005 | 0 | 1 | 1 |
| 2007 | 1 | 0 | 1 |
| 2008 | 1 | 1 | 2 |
| 2009 | 1 | 1 | 2 |
| 2010 | 0 | 2 | 2 |
| 2011 | 0 | 3 | 3 |
| 2012 | 1 | 3 | 4 |
| 2013 | 1 | 2 | 3 |
| 2014 | 0 | 2 | 2 |
| 2015 | 0 | 2 | 2 |
| 2016 | 0 | 3 | 3 |
| 2017 | 0 | 1 | 1 |
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Below are the most recent publications written about "Smad Proteins" by people in Profiles.
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Silencing Med12 Gene Reduces Proliferation of Human Leiomyoma Cells Mediated via Wnt/ß-Catenin Signaling Pathway. Endocrinology. 2017 03 01; 158(3):592-603.
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Bone mesenchymal stem cell-conditioned medium induces the upregulation of Smad6, which inhibits the BMP-4/Smad1/5/8 signaling pathway. Neurol Res. 2016 Nov; 38(11):965-972.
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MnTBAP increases BMPR-II expression in endothelial cells and attenuates vascular inflammation. Vascul Pharmacol. 2016 09; 84:67-73.
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Constitutive Expression of a Dominant-Negative TGF-ß Type II Receptor in the Posterior Left Atrium Leads to Beneficial Remodeling of Atrial Fibrillation Substrate. Circ Res. 2016 06 24; 119(1):69-82.
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Sphingosine-1-phosphate lyase is an endogenous suppressor of pulmonary fibrosis: role of S1P signalling and autophagy. Thorax. 2015 Dec; 70(12):1138-48.
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All-Trans Retinoic Acid Induces TGF-ß2 in Intestinal Epithelial Cells via RhoA- and p38a MAPK-Mediated Activation of the Transcription Factor ATF2. PLoS One. 2015; 10(7):e0134003.
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Targeting latent TGFß release in muscular dystrophy. Sci Transl Med. 2014 Oct 22; 6(259):259ra144.
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ß-Arrestins regulate human cardiac fibroblast transformation and collagen synthesis in adverse ventricular remodeling. J Mol Cell Cardiol. 2014 Nov; 76:73-83.
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Recurrent somatic mutations in ACVR1 in pediatric midline high-grade astrocytoma. Nat Genet. 2014 May; 46(5):462-6.
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Oral administration of transforming growth factor-ß1 (TGF-ß1) protects the immature gut from injury via Smad protein-dependent suppression of epithelial nuclear factor ?B (NF-?B) signaling and proinflammatory cytokine production. J Biol Chem. 2013 Nov 29; 288(48):34757-66.