ArticleGenes & development2001
Smad3 recruits the anaphase-promoting complex for ubiquitination and degradation of SnoN.
Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
105 citing papers in PubMed, 218 citations in OpenAlex.
- The Anaphase-Promoting Complex/Cyclosome Is a Cellular Ageing Regulator.International journal of molecular sciences · 2022Review
- Arkadia-SKI/SnoN signaling differentially regulates TGF-β-induced iTreg and Th17 cell differentiation.The Journal of experimental medicine · 2021Article
- The importance of CDC27 in cancer: molecular pathology and clinical aspects.Cancer cell international · 2021Review
- Review
- The Influence of Adalimumab and Cyclosporine A on the Expression Profile of the Genes Related to TGFMediators of inflammation · 2020Article
- SnoN residue (1-366) attenuates hypertrophic scars through resistance to transforming growth factor-β1-induced degradation.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- The Transcriptional Regulator SnoN Promotes the Proliferation of Cerebellar Granule Neuron Precursors in the Postnatal Mouse Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- APC/CCellular and molecular life sciences : CMLS · 2019Article
- MicroRNA co-expression networks exhibit increased complexity in pancreatic ductal compared to Vater's papilla adenocarcinoma.Oncotarget · 2017Article
- New Functions of APC/C Ubiquitin Ligase in the Nervous System and Its Role in Alzheimer's Disease.International journal of molecular sciences · 2017Review
- The PIAS3-Smurf2 sumoylation pathway suppresses breast cancer organoid invasiveness.Oncotarget · 2017Article
- The APC/C Coordinates Retinal Differentiation with G1 Arrest through the Nek2-Dependent Modulation of Wingless Signaling.Developmental cell · 2017Article
- Posttranslational Regulation of Smads.Cold Spring Harbor perspectives in biology · 2016Review
- APC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathway.Bioscience reports · 2016Review
- TGF-β Signaling from Receptors to Smads.Cold Spring Harbor perspectives in biology · 2016Review
- Suppression of APC/CCdh1 has subtype specific biological effects in acute myeloid leukemia.Oncotarget · 2016Article
- The ubiquitin ligase Smurf2 suppresses TGFβ-induced epithelial-mesenchymal transition in a sumoylation-regulated manner.Cell death and differentiation · 2016Article
- A decade of the anaphase-promoting complex in the nervous system.Genes & development · 2016Review
- The influence of SnoN gene silencing by siRNA on the cell proliferation and apoptosis of human pancreatic cancer cells.Diagnostic pathology · 2015Article
- The regulation of TGF-β/SMAD signaling by protein deubiquitination.Protein & cell · 2014Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Smad proteins mediate transforming growth factor-beta (TGF-beta) signaling to regulate cell growth and differentiation. SnoN is an important negative regulator of TGF-beta signaling that functions to maintain the repressed state of TGF-beta target genes in the absence of ligand. On TGF-beta stimulation, Smad3 and Smad2 translocate into the nucleus and induce a rapid degradation of SnoN, allowing activation of TGF-beta target genes. We show that Smad2- or Smad3-induced degradation of SnoN requires the ubiquitin-dependent proteasome and can be mediated by the anaphase-promoting complex (APC) and the UbcH5 family of ubiquitin-conjugating enzymes. Smad3 and to a lesser extent, Smad2, interact with both the APC and SnoN, resulting in the recruitment of the APC to SnoN and subsequent ubiquitination of SnoN in a destruction box (D box)-dependent manner. In addition to the D box, efficient ubiquitination and degradation of SnoN also requires the Smad3 binding site in SnoN as well as key lysine residues necessary for ubiquitin attachment. Mutation of either the Smad3 binding site or lysine residues results in stabilization of SnoN and in enhanced antagonism of TGF-beta signaling. Our studies elucidate an important mechanism and pathway for the degradation of SnoN and more importantly, reveal a novel role of the APC in the regulation of TGF-beta signaling.
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Registered trials
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.