Integration of TGF‐β/Smad and Jagged1/Notch signalling in epithelial‐to‐mesenchymal transition

By Jiri Zavadil, L. Cermak, Noemí Soto-Nieves, Erwin P. Bottinger. 2004

690 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/b20ca9c4a9db50a93d63729fed396f92c3a72d93

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. R. Weinberg
2. R. Derynck
3. Raghu Kalluri
4. A. Moustakas
5. C. Heldin
6. Jing Yang
7. J. P. Thiery
8. E. Hay

In Oncology

1. R. Weinberg
2. R. Derynck
3. Raghu Kalluri
4. Jing Yang
5. E. Hay
6. J. P. Thiery
7. A. Moustakas
8. C. Heldin

Citations in the corpus

• Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. (2008, background): “Furthermore, in epithelial cells from the mammary gland, kidney tubules, and epidermis, the Notch ligand Jagged 1 and the Notch target Hey1 are induced by TGF-b at the onset of EMT in a Smad3-dependent fashion (Zavadil et al., 2004).”
• Non-Smad TGF-β signals (2005, background): “However, the EMT also depends on ERK activity, and pathways activated by oncogenic Ras or physiological Notch receptor signalling synergize with TGF-β (Oft et al., 1996; Oft et al., 1998; Zavadil et al., 2001; Jechlinger et al., 2003; Zavadil et al., 2004).”
• Notch signaling mediates hypoxia-induced tumor cell migration and invasion (2008, background): “Furthermore, Notch can up-regulate Snail-1 and induce EMT in normoxia during normal development in cardiac and kidney tubular cell differentiation (19, 20), although the detailed molecular mechanism for how Notch controls Snail-1 expression remains to be established.”
• EMT, the cytoskeleton, and cancer cell invasion (2009, background): “Among the candidates which are engaged by TGFβ-induced EMT are the small GTPases RhoA and Rac1 [12, 13], Ras [14], phosphoinositol–3 kinase (PI3K) [15], Mitogen-activated protein kinase (MAPK) [13], integrin-linked kinase (ILK) [16], and the Jagged1/Notch signaling pathway [17].”
• TGF-β and epithelial-to-mesenchymal transitions (2005, background): “…as it is observed in multiple cell types including human, murine and canine proximal tubular cells, mammary cells and immortalized keratinocytes (Zavadil et al., 2004), while it is not detectable in cells that do not undergo EMT in response to TGF-b, such as primary human keratinocytes (J…”
• The epithelial–mesenchymal transition: new insights in signaling, development, and disease (2006, background): “Zavadil used extensive gene expression profi ling to identify HEY1 targets that are important in EMT induction (Zavadil et al., 2004).”
• Notch signaling: simplicity in design, versatility in function (2011, background): “TGF-mediated epithelial-tomesenchymal transition (EMT) also requires functional Notch signaling in the developing heart (Timmerman et al., 2004) and in various epithelia (Niimi et al., 2007; Zavadil et al., 2004).”
• Notch signalling in solid tumours: a little bit of everything but not all the time (2011, background): “Furthermore, crosstalk between Notch and TGFβ is important for the initiation of EMT, as Notch signalling is required to sustain TGFβ-induced HEY1 expressio”