Smad transcription factors.

By J. Massagué, J. Seoane, D. Wotton. Genes & Development, 2005

2,527 citations recorded by the source corpus.

Smad transcription factors lie at the core of one of the most versatile cytokine signaling pathways in metazoan biology-the transforming growth factor-beta (TGFbeta) pathway. Recent progress has shed light into the processes of Smad activation and deactivation, nucleocytoplasmic dynamics, and assembly of transcriptional complexes. A rich repertoire of regulatory devices exerts control over each step of the Smad pathway. This knowledge is enabling work on more complex questions about the organization, integration, and modulation of Smad-dependent transcriptional programs. We are beginning to uncover self-enabled gene response cascades, graded Smad response mechanisms, and Smad-dependent synexpression groups. Our growing understanding of TGFbeta signaling through the Smad pathway provides general principles for how animal cells translate complex inputs into concrete behavior.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/aa11110f28aa3a968599cb4341bc7924da647a58

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In Molecular Biology

1. R. Gomis
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Citations in the corpus

• TGFbeta primes breast tumors for lung metastasis seeding through angiopoietin-like 4. (2008, neutral): “We perturbed the TGFβ pathway in LM2 cells by overexpressing a kinase-defective, dominant-negative mutant form of the TGFβ type I receptor (Weis-Garcia and Massagué, 1996), or by reducing the expression of Smad4, which is an essential partner of Smad2/3 in the formation of transcriptional complexes ”
• Cellular and Molecular Basis of Pulmonary Arterial Hypertension (2009, background): “Activated type I receptors in turn phosphorylate cytoplasmic signaling proteins known as Smads, which are responsible for TGF- superfamily signal transduction (83).”
• The logic of TGFβ signaling (2006, background): “powerful signaling process (for reviews see [29,30]).”
• Targeting cancer stem cell pathways for cancer therapy (2020, background): “343 Many studies have shown that activation of TGF/Smad signaling also occurs in human cancers.”
• Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression (2010, background): “TGF-β is a ubiquitously expressed cytokine that binds to a target cell through the type I and II TGF-β receptors, initiating multiple signaling cascades, including the canonical Smad signaling pathway, that ultimately regulate transcription in combination with cofactors [123].”
• Mutations in SMAD3 cause a syndromic form of aortic aneurysms and dissections with early-onset osteoarthritis (2011, background): “This gene encodes a member of the TGF-β pathway that is essential for TGF-β signal transmissio”
• Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update. (2012, background): “by the TGF- receptor, thereby reducing the potency of TGF- receptor signaling (189, 264).”
• Formation and function of the myofibroblast during tissue repair. (2007, background): “The serine/threonine kinase activity of the activated complex phosphorylates Smad2 and Smad3, that each bind to Smad4 and translocate into the nucleus to enhance gene transcription by cooperating with DNA transcription factors (Feng and Derynck, 2005; Massague et al., 2005).”
• Master Transcription Factors Determine Cell-Type-Specific Responses to TGF-β Signaling (2011, neutral): “If many different transcription factors can interact with Smad2/3 (Chen et al., 1996, 2002, 1997; Germain et al., 2000; Liu et al., 1997; Massagué et al., 2005; Seoane, 2004), why do master transcription factors have such a profound effect in determining the genes regulated by TGF-b signaling in eac”