ArticleMethods in molecular biology (Clifton, N.J.)2010
Coupling of dephosphorylation and nuclear export of Smads in TGF-beta signaling.
Article in Methods in molecular biology (Clifton, N.J.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- Platyconic acid A‑induced PPM1A upregulation inhibits the proliferation, inflammation and extracellular matrix deposition of TGF‑β1‑induced lung fibroblasts.Molecular medicine reports · 2022Article
- Nuclear Transport and Accumulation of Smad Proteins Studied by Single-Molecule Microscopy.Biophysical journal · 2018Article
- HOXA13 is a potential GBM diagnostic marker and promotes glioma invasion by activating the Wnt and TGF-β pathways.Oncotarget · 2015Article
- Nuclear Export of Smads by RanBP3L Regulates Bone Morphogenetic Protein Signaling and Mesenchymal Stem Cell Differentiation.Molecular and cellular biology · 2015Article
- Loss of PPM1A expression enhances invasion and the epithelial-to-mesenchymal transition in bladder cancer by activating the TGF-β/Smad signaling pathway.Oncotarget · 2014Article
- Integrating developmental signals: a Hippo in the (path)way.Oncogene · 2012Review
- Key signaling nodes in mammary gland development and cancer: Smad signal integration in epithelial cell plasticity.Breast cancer research : BCR · 2012Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In eukaryotes, regulation of signaling mediators/effectors in the nucleus is one of the principal mechanisms that govern duration and strength of signaling. Smads are a family of structurally related intracellular proteins that serve as signaling effectors for transforming growth factor beta (TGF-beta) and TGF-beta-related proteins. Accumulating evidence demonstrates that Smads possess intrinsic nucleocytoplasmic shuttling capacity, which enables them to transmit TGF-beta signals from cell membrane to nucleus. We recently identified two important steps in the termination of nuclear Smad signaling. The first step is initiated by a serine/threonine phosphatase PPM1A that dephosphorylates Smad2/3 in the nucleus, thereby shutting down signaling capacity of phosphorylated Smad2/3. The second step involves nuclear export of dephosphorylated Smad2/3 with the aid of nuclear protein RanBP3 to terminate Smad signaling. This chapter introduces methods for examining nuclear export of Smad2/3 in 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.