ArticlePloS one2013
Four amino acids within a tandem QxVx repeat in a predicted extended α-helix of the Smad-binding domain of Sip1 are necessary for binding to activated Smad proteins.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
The trial behind it
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Dualistic role of ZEB1 and ZEB2 in tumor progression.Biology direct · 2025Review
- ZEB2 Gene Pathogenic Variants Across Protein-Coding Regions and Impact on Clinical Manifestations: A Review.International journal of molecular sciences · 2025Review
- Review
- Zeb2 regulates the balance between retinal interneurons and Müller glia by inhibition of BMP-Smad signaling.Developmental biology · 2020Article
- Targeted chromatin conformation analysis identifies novel distal neural enhancers of ZEB2 in pluripotent stem cell differentiation.Human molecular genetics · 2020Article
- Zeb2 Regulates Myogenic Differentiation in Pluripotent Stem Cells.International journal of molecular sciences · 2020Article
- Nonfunctional Missense Mutants in Two Well Characterized Cytosolic Enzymes Reveal Important Information About Protein Structure and Function.The protein journal · 2018Article
- Zeb2 is a negative regulator of midbrain dopaminergic axon growth and target innervation.Scientific reports · 2017Article
- RGC32 induces epithelial-mesenchymal transition by activating the Smad/Sip1 signaling pathway in CRC.Scientific reports · 2017Article
- Aptamers and their potential to selectively target aspects of EGF, Wnt/β-catenin and TGFβ-smad family signaling.International journal of molecular sciences · 2013Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The zinc finger transcription factor Smad-interacting protein-1 (Sip1; Zeb2, Zfhx1b) plays an important role during vertebrate embryogenesis in various tissues and differentiating cell types, and during tumorigenesis. Previous biochemical analysis suggests that interactions with several partner proteins, including TGFβ family receptor-activated Smads, regulate the activities of Sip1 in the nucleus both as a DNA-binding transcriptional repressor and activator. Using a peptide aptamer approach we mapped in Sip1 its Smad-binding domain (SBD), initially defined as a segment of 51 amino acids, to a shorter stretch of 14 amino acids within this SBD. Modelling suggests that this short SBD stretch is part of an extended α-helix that may fit the binding to a hydrophobic corridor within the MH2 domain of activated Smads. Four amino acids (two polar Q residues and two non-polar V residues) that form the tandem repeat (QxVx)2 in this 14-residue stretch were found to be crucial for binding to both TGFβ/Nodal/Activin-Smads and BMP-Smads. A full-length Sip1 with collective mutation of these Q and V residues (to A) no longer binds to Smads, while it retains its binding activity to its cognate bipartite target DNA sequence. This missense mutant Sip1(AxAx)2 provides a new molecular tool to identify SBD (in)dependent target genes in Sip1-controlled TGFβ and/or BMP (de)regulated cellular, developmental and pathological processes.
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