Transcriptional control by the TGF‐β/Smad signaling system

By J. Massagué, D. Wotton. 2000

1,683 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/8ce8139e81f88cd3e9a28b0be719c6600b1c098f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Massagué
2. J. Seoane
3. D. Wotton
4. H. Lan
5. Xiao-ming Meng
6. P. Tang
7. Jun Li
8. Lei Zhang

In Oncology

1. J. Massagué
2. J. Seoane
3. D. Wotton
4. Changwei Liu
5. Fengyun Xu
6. Lei Zhang
7. Dan-dan Zhou
8. H. Lan

Citations in the corpus

• TGF-β/SMAD Pathway and Its Regulation in Hepatic Fibrosis (2016, positive): “The TGF-β superfamily includes a large number of structurally and functionally related proteins, such as bone morphogenetic proteins (BMPs), activins, inhibins, growth differentiation factors (GDFs), and glial-derived neurotrophic factors (GDNFs) (Maribo et al. 1998; Massague and Wotton 2000).”
• Hypoxia and the hypoxia-inducible-factor pathway in glioma growth and angiogenesis. (2005, neutral): “Upon activation, SMADs translocate to the nucleus, where they require interaction with various DNA binding cofactors to specify the cell’s diverse responses to TGF(Massague and Wotton, 2000).”
• Ras and TGFβ cooperatively regulate epithelial cell plasticity and metastasis (2002, positive): “Therefore, the MAPK pathway might attenuate TGF responses via the induction and/or activation of new distinct transcription factors, corepressors, or coactivators recruited by Smads into a variety of transcriptional modules, which determine the diversity of responses to similar TGF signals in differ”
• Smad transcription factors. (2005, positive): “This mode of interaction provides a basis for high affinity and selectivity in the recognition of target genes and a venue for the differential action of TGF in different cell types (Massagué and Wotton 2000).”
• SB-431542 is a potent and specific inhibitor of transforming growth factor-beta superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7. (2002, neutral): “The activated Smad complexes accumulate in the nucleus, where they are directly involved in the transcription of target genes, usually in association with other specific DNA-binding transcription factors (Massagué and Wotton, 2000).”