"Smad3 Protein" 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 receptor-regulated smad protein that undergoes PHOSPHORYLATION by ACTIVIN RECEPTORS, TYPE I. Activated Smad3 can bind directly to DNA, and it regulates TRANSFORMING GROWTH FACTOR BETA and ACTIVIN signaling.
Descriptor ID |
D051900
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MeSH Number(s) |
D12.644.360.024.334.500.300 D12.776.157.057.170.500.300 D12.776.260.713.500.300 D12.776.476.024.428.500.300 D12.776.744.741.875 D12.776.930.806.500.300
|
Concept/Terms |
|
Below are MeSH descriptors whose meaning is more general than "Smad3 Protein".
- Chemicals and Drugs [D]
- Amino Acids, Peptides, and Proteins [D12]
- Peptides [D12.644]
- Intracellular Signaling Peptides and Proteins [D12.644.360]
- Adaptor Proteins, Signal Transducing [D12.644.360.024]
- Smad Proteins [D12.644.360.024.334]
- Smad Proteins, Receptor-Regulated [D12.644.360.024.334.500]
- Smad3 Protein [D12.644.360.024.334.500.300]
- Proteins [D12.776]
- Carrier Proteins [D12.776.157]
- Adaptor Proteins, Signal Transducing [D12.776.157.057]
- Smad Proteins [D12.776.157.057.170]
- Smad Proteins, Receptor-Regulated [D12.776.157.057.170.500]
- Smad3 Protein [D12.776.157.057.170.500.300]
- DNA-Binding Proteins [D12.776.260]
- Smad Proteins [D12.776.260.713]
- Smad Proteins, Receptor-Regulated [D12.776.260.713.500]
- Smad3 Protein [D12.776.260.713.500.300]
- Intracellular Signaling Peptides and Proteins [D12.776.476]
- Adaptor Proteins, Signal Transducing [D12.776.476.024]
- Smad Proteins [D12.776.476.024.428]
- Smad Proteins, Receptor-Regulated [D12.776.476.024.428.500]
- Smad3 Protein [D12.776.476.024.428.500.300]
- Phosphoproteins [D12.776.744]
- Smad Proteins, Receptor-Regulated [D12.776.744.741]
- Smad3 Protein [D12.776.744.741.875]
- Transcription Factors [D12.776.930]
- Smad Proteins [D12.776.930.806]
- Smad Proteins, Receptor-Regulated [D12.776.930.806.500]
- Smad3 Protein [D12.776.930.806.500.300]
Below are MeSH descriptors whose meaning is more specific than "Smad3 Protein".
This graph shows the total number of publications written about "Smad3 Protein" by people in this website by year, and whether "Smad3 Protein" 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 |
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2004 | 0 | 2 | 2 |
2005 | 0 | 2 | 2 |
2007 | 0 | 2 | 2 |
2008 | 1 | 1 | 2 |
2009 | 1 | 0 | 1 |
2010 | 1 | 0 | 1 |
2011 | 0 | 1 | 1 |
2012 | 1 | 0 | 1 |
2013 | 0 | 1 | 1 |
2014 | 0 | 1 | 1 |
2015 | 1 | 1 | 2 |
2017 | 0 | 2 | 2 |
2019 | 0 | 2 | 2 |
2024 | 0 | 1 | 1 |
To return to the timeline,
click here.
Below are the most recent publications written about "Smad3 Protein" by people in Profiles.
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Integrative Multiomics in the Lung Reveals a Protective Role of Asporin in Pulmonary Arterial Hypertension. Circulation. 2024 Oct 15; 150(16):1268-1287.
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Oocyte-Secreted Factors Synergize With FSH to Promote Aromatase Expression in Primary Human Cumulus Cells. J Clin Endocrinol Metab. 2019 05 01; 104(5):1667-1676.
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Sustained Smad2 Phosphorylation Is Required for Myofibroblast Transformation in Response to TGF-ß. Am J Respir Cell Mol Biol. 2019 03; 60(3):367-369.
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Regulation of AMH by oocyte-specific growth factors in human primary cumulus cells. Reproduction. 2017 12; 154(6):745-753.
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The kielin/chordin-like protein (KCP) attenuates high-fat diet-induced obesity and metabolic syndrome in mice. J Biol Chem. 2017 06 02; 292(22):9051-9062.
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Epigenome-wide analysis links SMAD3 methylation at birth to asthma in children of asthmatic mothers. J Allergy Clin Immunol. 2017 Aug; 140(2):534-542.
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SIRT3 Blocks Aging-Associated Tissue Fibrosis in Mice by Deacetylating and Activating Glycogen Synthase Kinase 3ß. Mol Cell Biol. 2015 Dec 14; 36(5):678-92.
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Smad3 Signaling Promotes Fibrosis While Preserving Cardiac and Aortic Geometry in Obese Diabetic Mice. Circ Heart Fail. 2015 Jul; 8(4):788-98.
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Deficiency of cardiomyocyte-specific microRNA-378 contributes to the development of cardiac fibrosis involving a transforming growth factor ß (TGFß1)-dependent paracrine mechanism. J Biol Chem. 2014 Sep 26; 289(39):27199-27215.
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Excess SMAD signaling contributes to heart and muscle dysfunction in muscular dystrophy. Hum Mol Genet. 2014 Dec 20; 23(25):6722-31.