"Smad2 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. It regulates TRANSFORMING GROWTH FACTOR BETA and ACTIVIN signaling.
Descriptor ID |
D051899
|
MeSH Number(s) |
D12.644.360.024.334.500.200 D12.776.157.057.170.500.200 D12.776.476.024.428.500.200 D12.776.744.741.750 D12.776.930.806.500.200
|
Concept/Terms |
Smad2 Protein- Smad2 Protein
- MAD-Related 2 Protein
- MAD Related 2 Protein
- MADR2 Protein
|
Below are MeSH descriptors whose meaning is more general than "Smad2 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]
- Smad2 Protein [D12.644.360.024.334.500.200]
- 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]
- Smad2 Protein [D12.776.157.057.170.500.200]
- 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]
- Smad2 Protein [D12.776.476.024.428.500.200]
- Phosphoproteins [D12.776.744]
- Smad Proteins, Receptor-Regulated [D12.776.744.741]
- Smad2 Protein [D12.776.744.741.750]
- Transcription Factors [D12.776.930]
- Smad Proteins [D12.776.930.806]
- Smad Proteins, Receptor-Regulated [D12.776.930.806.500]
- Smad2 Protein [D12.776.930.806.500.200]
Below are MeSH descriptors whose meaning is more specific than "Smad2 Protein".
This graph shows the total number of publications written about "Smad2 Protein" by people in this website by year, and whether "Smad2 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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1998 | 0 | 1 | 1 |
1999 | 0 | 2 | 2 |
2000 | 0 | 2 | 2 |
2001 | 0 | 2 | 2 |
2002 | 0 | 2 | 2 |
2004 | 0 | 3 | 3 |
2005 | 0 | 4 | 4 |
2006 | 2 | 2 | 4 |
2007 | 0 | 3 | 3 |
2008 | 2 | 4 | 6 |
2009 | 2 | 3 | 5 |
2010 | 1 | 2 | 3 |
2011 | 1 | 3 | 4 |
2012 | 0 | 1 | 1 |
2013 | 0 | 1 | 1 |
2014 | 0 | 1 | 1 |
2015 | 0 | 2 | 2 |
2016 | 2 | 0 | 2 |
2017 | 2 | 0 | 2 |
2018 | 1 | 1 | 2 |
2019 | 1 | 2 | 3 |
2020 | 0 | 1 | 1 |
2021 | 0 | 1 | 1 |
2024 | 1 | 1 | 2 |
To return to the timeline,
click here.
Below are the most recent publications written about "Smad2 Protein" by people in Profiles.
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BATF is a major driver of NK cell epigenetic reprogramming and dysfunction in AML. Sci Transl Med. 2024 Sep 11; 16(764):eadp0004.
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Thbs1 regulates skeletal muscle mass in a TGF?-Smad2/3-ATF4-dependent manner. Cell Rep. 2024 May 28; 43(5):114149.
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Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium. J Mol Cell Cardiol. 2022 10; 171:1-15.
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Haploinsufficiency of Tmem43 in cardiac myocytes activates the DNA damage response pathway leading to a late-onset senescence-associated pro-fibrotic cardiomyopathy. Cardiovasc Res. 2021 09 28; 117(11):2377-2394.
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The role of Smad2 and Smad3 in regulating homeostatic functions of fibroblasts in vitro and in adult mice. Biochim Biophys Acta Mol Cell Res. 2020 07; 1867(7):118703.
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Targeting the E3 Ubiquitin Ligase PJA1 Enhances Tumor-Suppressing TGF? Signaling. Cancer Res. 2020 05 01; 80(9):1819-1832.
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Genetic and molecular mechanism for distinct clinical phenotypes conveyed by allelic truncating mutations implicated in FBN1. Mol Genet Genomic Med. 2020 01; 8(1):e1023.
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Distinct roles of myofibroblast-specific Smad2 and Smad3 signaling in repair and remodeling of the infarcted heart. J Mol Cell Cardiol. 2019 07; 132:84-97.
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Reply to Liu et al.: ALK5-mediated tumor suppressor signaling through SMAD2 and SMAD3 in the uterus. Proc Natl Acad Sci U S A. 2019 05 07; 116(19):9166-9167.
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Uterine double-conditional inactivation of Smad2 and Smad3 in mice causes endometrial dysregulation, infertility, and uterine cancer. Proc Natl Acad Sci U S A. 2019 02 26; 116(9):3873-3882.