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Article

Specific interactions between Smad proteins and AP-1 components determine TGFβ-induced breast cancer cell invasion

27 Aug 2012

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Identifiers

PMID: 22926518
DOI: 10.1038/onc.2012.370

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Specific interactions between Smad proteins and AP-1 components determine TGFβ-induced breast cancer cell invasionPMID 22926518Read ↗

Smad3/AP-1 interactions control transcriptional responses to TGF-β in a promoter-specific mannerSemantic proximity Read ↗

Genome-wide mechanisms of Smad bindingSemantic proximity Read ↗

TGFβ Signaling: Receptors, Transducers, and Mad ProteinsSemantic proximity Read ↗

SMADs: mediators and regulators of TGF-β signalingSemantic proximity Read ↗

Crosstalk between TGF-β signaling and miRNAs in breast cancer metastasisSemantic proximity Read ↗

SMAD Proteins in TGF-β Signalling Pathway in Cancer: Regulatory Mechanisms and Clinical ApplicationsSemantic proximity Read ↗

TGF-β SIGNAL TRANSDUCTIONSemantic proximity Read ↗

Identification of a PEAK1/ZEB1 signaling axis during TGFβ/fibronectin-induced EMT in breast cancerSemantic proximity Read ↗

TGF‐β signaling: A recap of SMAD‐independent and SMAD‐dependent pathwaysSemantic proximity Read ↗

A SNAIL1–SMAD3/4 transcriptional repressor complex promotes TGF-β mediated epithelial–mesenchymal transitionSemantic proximity Read ↗

Cooperative Assembly of TGF-β Superfamily Signaling Complexes Is Mediated by Two Disparate Mechanisms and Distinct Modes of Receptor BindingSemantic proximity Read ↗

Transcriptional Activators of TGF-β Responses: SmadsSemantic proximity Read ↗

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