ArticleMolecular and cellular biology2001
Mechanism for mutational inactivation of the tumor suppressor Smad2.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- The Activation Status of the TGF-β Transducer Smad2 Is Associated with a Reduced Survival in Gastrointestinal Cancers: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2019Pooled it
- SMAD2 rs4940086 heterozygosity increases the risk of cervical cancer development among the women in Bangladesh.Molecular biology reports · 2020Article
- GDF11/BMP11 as a novel tumor marker for liver cancer.Experimental and therapeutic medicine · 2018Article
- The orphan GPR50 receptor promotes constitutive TGFβ receptor signaling and protects against cancer development.Nature communications · 2018Article
- Metabolic derivatives of alcohol and the molecular culprits of fibro-hepatocarcinogenesis: Allies or enemies?World journal of gastroenterology · 2016Review
- Efficient retina formation requires suppression of both Activin and BMP signaling pathways in pluripotent cells.Biology open · 2015Article
- Alterations in the Smad pathway in human cancers.Frontiers in bioscience (Landmark edition) · 2012Review
- CCN5, a novel transcriptional repressor of the transforming growth factor β signaling pathway.Molecular and cellular biology · 2011Article
- Identification of PCTA, a TGIF antagonist that promotes PML function in TGF-beta signalling.The EMBO journal · 2008Article
- Bcr-Abl activates the AKT/Fox O3 signalling pathway to restrict transforming growth factor-beta-mediated cytostatic signals.EMBO reports · 2005Article
- The novel E3 ubiquitin ligase Tiul1 associates with TGIF to target Smad2 for degradation.The EMBO journal · 2004Article
- Article
- Identifying disease genes and module biomarkers by differential interactions.Journal of the American Medical Informatics Association : JAMIAArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor beta (TGF-beta) is a potent natural antiproliferative agent that plays an important role in suppressing tumorigenicity. In numerous tumors, loss of TGF-beta responsiveness is associated with inactivating mutations that can occur in components of this signaling pathway, such as the tumor suppressor Smad2. Although a general framework for how Smads transduce TGF-beta signals has been proposed, the physiological relevance of alterations of Smad2 functions in promoting tumorigenesis is still unknown. Here, we show that expression of Smad2.P445H, a tumor-derived mutation of Smad2 found in human cancer, suppresses the ability of the Smads to mediate TGF-beta-induced growth arrest and transcriptional responses. Smad2.P445H is phosphorylated by the activated TGF-beta receptor at the carboxy-terminal serine residues and associates with Smad3 and Smad4 but is unable to dissociate from the receptor. Upon ligand-induced phosphorylation, Smad2.P445H interacts stably with wild-type Smad2, thereby blocking TGF-beta-induced nuclear accumulation of wild-type Smad2 and Smad2-dependent transcription. The ability of the Smad2.P445H to block the nuclear accumulation of wild-type Smad2 protein reveals a new mechanism for loss of sensitivity to the growth-inhibitory functions of TGF-beta in tumor development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.