TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transition.

By Ulrich Valcourt, M. Kowanetz, Hideki Niimi, C. Heldin, A. Moustakas. Molecular Biology of the Cell, 2005

644 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/73dc401deeedc71b25e8c48fffc2e8467c759009

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. C. Heldin
2. A. Moustakas
3. Angeliki Voulgari
4. A. Pintzas
5. Jiri Zavadil
6. Erwin P. Bottinger
7. R. Derynck

In Oncology

1. Angeliki Voulgari
2. A. Pintzas
3. C. Heldin
4. A. Moustakas
5. R. Derynck

In Pathology and Forensic Medicine

1. Angeliki Voulgari
2. A. Pintzas

Citations in the corpus

• TGF-β and epithelial-to-mesenchymal transitions (2005, background): “Overexpression of inhibitory Smad7 consistently blocks Smad3-dependent EMT in vitro, including retinal pigment epithelium (Saika et al., 2004b), mammary epithelial cells (Valcourt et al., 2005), and in the renal UUO model in vivo (Lan et al., 2003).”
• Direct Signaling Between Platelets and Cancer Cells Induces an Epithelial-Mesenchymal-Like Transition and Promotes Metastasis (2011, neutral): “, 2009) VALCOURT_TGFB (Valcourt et al., 2005) HINATA_NFKB_TARGETS_KERATINOCYTE MSigDB, (Hinata et al.”
• Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “transient state resembling EMT in normal epithelial cells [132] whereas in other cell types, cell mutations finally affecting the”
• Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition. (2005, background): “For example, when normal epithelial cells were exposed to transforming growth factor h1 in vitro , the resulting EMT was associated with a marked reduction of [(3)H]thymidine incorporation (25).”
• Non-Smad TGF-β signals (2005, background): “The Smads, especially Smad3 and Smad4, are critical for the EMT response not only in vitro (Valcourt et al., 2005), but also in vivo, for aggressive carcinoma metastasis and lens EMT (Oft et al., 2002; Li et al., 2003; Tian et al., 2003; Saika et al., 2004; Tian et al., 2004).”
• Chronic Inflammation and Cytokines in the Tumor Microenvironment (2014, background): “The immune response comprises a series of events triggered in response to recognition of pathogens or tissue damage, involving cells and soluble mediators, such as cytokines of”