JNK mediates TGF-beta1-induced epithelial mesenchymal transdifferentiation of mouse transformed keratinocytes (Q40229029)

18 September 2017

title

JNK mediates TGF-beta1-induced epithelial mesenchymal transdifferentiation of mouse transformed keratinocytes (English)

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18 September 2017

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Juan F Santibañez

1

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18 September 2017

language of work or name

English

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publication date

12 September 2006

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18 September 2017

number of pages

7

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based on heuristic

inferred from page(s)

published in

FEBS Letters

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18 September 2017

volume

580

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18 September 2017

issue

22

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18 September 2017

page(s)

5385-5391

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18 September 2017

cites work

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Smad-dependent and Smad-independent pathways in TGF-beta family signalling

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Blockade of Smad4 in transformed keratinocytes containing a Ras oncogene leads to hyperactivation of the Ras-dependent Erk signalling pathway associated with progression to undifferentiated carcinomas

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Involvement of the Ras/MAPK signaling pathway in the modulation of urokinase production and cellular invasiveness by transforming growth factor-beta(1) in transformed keratinocytes.

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TGFbeta signaling is necessary for carcinoma cell invasiveness and metastasis

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TGF-beta1 and Ha-Ras collaborate in modulating the phenotypic plasticity and invasiveness of epithelial tumor cells

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Transcriptional activation of the matrix metalloproteinase-9 gene in an H-ras and v-myc transformed rat embryo cell line

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Requirement of TGF-beta receptor-dependent activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases (Sapks) for TGF-beta up-regulation of the urokinase-type plasminogen activator receptor

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Transforming growth factor-beta1-dependent urokinase up-regulation and promotion of invasion are involved in Src-MAPK-dependent signaling in human ovarian cancer cells

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TGF-beta induces fibronectin synthesis through a c-Jun N-terminal kinase-dependent, Smad4-independent pathway

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The p150-Spir protein provides a link between c-Jun N-terminal kinase function and actin reorganization

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The role of the cell-adhesion molecule E-cadherin as a tumour-suppressor gene

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Co-expression of tenascin-C and vimentin in human breast cancer cells indicates phenotypic transdifferentiation during tumour progression: correlation with histopathological parameters, hormone receptors, and oncoproteins

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10.1016/J.FEBSLET.2006.09.003

21 January 2018

Identifiers

DOI

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18 September 2017

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