Activation of a Nodal-independent signaling pathway by Cripto-1 mutants with impaired activation of a Nodal-dependent signaling pathway

Caterina Bianco, Margaret Mysliwiec, Kazuhide Watanabe, Mario Mancino, Tadahiro Nagaoka, Monica Gonzales, David S. Salomon

Research output: Contribution to journal › Article

9 Citations (Scopus)

Abstract

Cripto-1, a co-receptor for Nodal, can activate Nodal-dependent and Nodal-independent signaling pathways. In this study we have investigated whether Cripto-1 mutants, that fail to activate a Nodal-dependent signaling pathway, are capable to activate a Nodal-independent signaling pathway in mammary epithelial cells. Cripto-1 mutants expressed in EpH4 mouse mammary epithelial cells are fully functional in regard to activation of a Nodal-independent signaling pathway, leading to phosphorylation of mitogen-activated protein kinase (MAPK) and Akt and to enhanced proliferation and motility of these cells, suggesting that Cripto-1 mutants with impaired Nodal signaling are still active in a Nodal-independent signaling pathway. Structured summary: MINT-6797299:Glypican 1 (uniprotkb:P35052) physically interacts (MI:0218) with Cr 1 (uniprotkb:P13385) by anti bait coimmunoprecipitation (MI:0006).

Original languageEnglish
Pages (from-to)3997-4002
Number of pages6
JournalFEBS Letters
Volume582
Issue number29
DOIs
Publication statusPublished - 10-12-2008
Externally publishedYes

Fingerprint

Breast
Epithelial Cells
Chemical activation
Glypicans
Mitogen-Activated Protein Kinases
Cell Movement
Phosphorylation
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • Structural Biology
  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Bianco, Caterina ; Mysliwiec, Margaret ; Watanabe, Kazuhide ; Mancino, Mario ; Nagaoka, Tadahiro ; Gonzales, Monica ; Salomon, David S. / Activation of a Nodal-independent signaling pathway by Cripto-1 mutants with impaired activation of a Nodal-dependent signaling pathway. In: FEBS Letters. 2008 ; Vol. 582, No. 29. pp. 3997-4002.
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abstract = "Cripto-1, a co-receptor for Nodal, can activate Nodal-dependent and Nodal-independent signaling pathways. In this study we have investigated whether Cripto-1 mutants, that fail to activate a Nodal-dependent signaling pathway, are capable to activate a Nodal-independent signaling pathway in mammary epithelial cells. Cripto-1 mutants expressed in EpH4 mouse mammary epithelial cells are fully functional in regard to activation of a Nodal-independent signaling pathway, leading to phosphorylation of mitogen-activated protein kinase (MAPK) and Akt and to enhanced proliferation and motility of these cells, suggesting that Cripto-1 mutants with impaired Nodal signaling are still active in a Nodal-independent signaling pathway. Structured summary: MINT-6797299:Glypican 1 (uniprotkb:P35052) physically interacts (MI:0218) with Cr 1 (uniprotkb:P13385) by anti bait coimmunoprecipitation (MI:0006).",
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Bianco, C, Mysliwiec, M, Watanabe, K, Mancino, M, Nagaoka, T, Gonzales, M & Salomon, DS 2008, 'Activation of a Nodal-independent signaling pathway by Cripto-1 mutants with impaired activation of a Nodal-dependent signaling pathway', FEBS Letters, vol. 582, no. 29, pp. 3997-4002. https://doi.org/10.1016/j.febslet.2008.10.052

Activation of a Nodal-independent signaling pathway by Cripto-1 mutants with impaired activation of a Nodal-dependent signaling pathway. / Bianco, Caterina; Mysliwiec, Margaret; Watanabe, Kazuhide; Mancino, Mario; Nagaoka, Tadahiro; Gonzales, Monica; Salomon, David S.

In: FEBS Letters, Vol. 582, No. 29, 10.12.2008, p. 3997-4002.

Research output: Contribution to journal › Article

TY - JOUR

T1 - Activation of a Nodal-independent signaling pathway by Cripto-1 mutants with impaired activation of a Nodal-dependent signaling pathway

AU - Bianco, Caterina

AU - Mysliwiec, Margaret

AU - Watanabe, Kazuhide

AU - Mancino, Mario

AU - Nagaoka, Tadahiro

AU - Gonzales, Monica

AU - Salomon, David S.

PY - 2008/12/10

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N2 - Cripto-1, a co-receptor for Nodal, can activate Nodal-dependent and Nodal-independent signaling pathways. In this study we have investigated whether Cripto-1 mutants, that fail to activate a Nodal-dependent signaling pathway, are capable to activate a Nodal-independent signaling pathway in mammary epithelial cells. Cripto-1 mutants expressed in EpH4 mouse mammary epithelial cells are fully functional in regard to activation of a Nodal-independent signaling pathway, leading to phosphorylation of mitogen-activated protein kinase (MAPK) and Akt and to enhanced proliferation and motility of these cells, suggesting that Cripto-1 mutants with impaired Nodal signaling are still active in a Nodal-independent signaling pathway. Structured summary: MINT-6797299:Glypican 1 (uniprotkb:P35052) physically interacts (MI:0218) with Cr 1 (uniprotkb:P13385) by anti bait coimmunoprecipitation (MI:0006).

AB - Cripto-1, a co-receptor for Nodal, can activate Nodal-dependent and Nodal-independent signaling pathways. In this study we have investigated whether Cripto-1 mutants, that fail to activate a Nodal-dependent signaling pathway, are capable to activate a Nodal-independent signaling pathway in mammary epithelial cells. Cripto-1 mutants expressed in EpH4 mouse mammary epithelial cells are fully functional in regard to activation of a Nodal-independent signaling pathway, leading to phosphorylation of mitogen-activated protein kinase (MAPK) and Akt and to enhanced proliferation and motility of these cells, suggesting that Cripto-1 mutants with impaired Nodal signaling are still active in a Nodal-independent signaling pathway. Structured summary: MINT-6797299:Glypican 1 (uniprotkb:P35052) physically interacts (MI:0218) with Cr 1 (uniprotkb:P13385) by anti bait coimmunoprecipitation (MI:0006).

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Bianco C, Mysliwiec M, Watanabe K, Mancino M, Nagaoka T, Gonzales M et al. Activation of a Nodal-independent signaling pathway by Cripto-1 mutants with impaired activation of a Nodal-dependent signaling pathway. FEBS Letters. 2008 Dec 10;582(29):3997-4002. https://doi.org/10.1016/j.febslet.2008.10.052

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