ArticleProceedings of the National Academy of Sciences of the United States of America2005
Cytoplasmic SnoN in normal tissues and nonmalignant cells antagonizes TGF-beta signaling by sequestration of the Smad proteins.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 78 citations in OpenAlex.
- SMAD2/3-SMYD2 and developmental transcription factors cooperate with cell-cycle inhibitors to guide tissue formation.Protein & cell · 2025Article
- Modeling Cellular Signaling Variability Based on Single-Cell Data: The TGFβ-SMAD Signaling Pathway.Methods in molecular biology (Clifton, N.J.) · 2023Review
- MAB21L4 regulates the TGF-β-induced expression of target genes in epidermal keratinocytes.Journal of biochemistry · 2022Article
- Molecular mechanism of smurf2 in regulating the expression of SnoN in diabetic nephropathy.Molecular medicine reports · 2017Article
- SnoN Antagonizes the Hippo Kinase Complex to Promote TAZ Signaling during Breast Carcinogenesis.Developmental cell · 2016Article
- Oxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF-β1/Smad Signaling Pathway.PloS one · 2016Article
- Novel regulation of Ski protein stability and endosomal sorting by actin cytoskeleton dynamics in hepatocytes.The Journal of biological chemistry · 2015Article
- The self-limiting dynamics of TGF-β signaling in silico and in vitro, with negative feedback through PPM1A upregulation.PLoS computational biology · 2014Article
- Molecular mechanisms of thoracic aortic dissection.The Journal of surgical research · 2013Review
- SnoN facilitates ALK1-Smad1/5 signaling during embryonic angiogenesis.The Journal of cell biology · 2013Article
- Expression profiles of SnoN in normal and cancerous human tissues support its tumor suppressor role in human cancer.PloS one · 2013Article
- SnoN regulates mammary gland alveologenesis and onset of lactation by promoting prolactin/Stat5 signaling.Development (Cambridge, England) · 2012Article
- SnoN suppresses maturation of chondrocytes by mediating signal cross-talk between transforming growth factor-β and bone morphogenetic protein pathways.The Journal of biological chemistry · 2012Article
- Transforming growth factor-β/SMAD Target gene SKIL is negatively regulated by the transcriptional cofactor complex SNON-SMAD4.The Journal of biological chemistry · 2012Article
- SnoN in regulation of embryonic development and tissue morphogenesis.FEBS letters · 2012Review
- Post-translational regulation of TGF-β receptor and Smad signaling.FEBS letters · 2012Review
- SnoN signaling in proliferating cells and postmitotic neurons.FEBS letters · 2012Review
- Intercellular variation in signaling through the TGF-β pathway and its relation to cell density and cell cycle phase.Molecular & cellular proteomics : MCP · 2012Article
- Protein-tyrosine phosphatase 1B (PTP1B) deficiency confers resistance to transforming growth factor-β (TGF-β)-induced suppressor effects in hepatocytes.The Journal of biological chemistry · 2012Article
- SnoN oncoprotein enhances estrogen receptor-α transcriptional activity.Cellular signalling · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
TGF-beta is a ubiquitously expressed cytokine that signals through the Smad proteins to regulate many diverse cellular processes. SnoN is an important negative regulator of Smad signaling. It has been described as a nuclear protein, based on studies of ectopically expressed SnoN and endogenous SnoN in cancer cell lines. In the nucleus, SnoN binds to Smad2, Smad3, and Smad4 and represses their ability to activate transcription of TGF-beta target genes through multiple mechanisms. Here, we show that, whereas SnoN is localized exclusively in the nucleus in cancer tissues or cells, in normal tissues and nontumorigenic or primary epithelial cells, SnoN is predominantly cytoplasmic. Upon morphological differentiation or cell-cycle arrest, SnoN translocates into the nucleus. In contrast to nuclear SnoN that represses the transcriptional activity of the Smad complexes, cytoplasmic SnoN antagonizes TGF-beta signaling by sequestering the Smad proteins in the cytoplasm. Interestingly, cytoplasmic SnoN is resistant to TGF-beta-induced degradation and therefore is more potent than nuclear SnoN in repressing TGF-beta signaling. Thus, we have identified a mechanism of regulation of TGF-beta signaling via differential subcellular localization of SnoN that is likely to produce different patterns of downstream TGF-beta responses and may influence the proliferation or differentiation states of epithelial cells.
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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.