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The Role of Wnt Signalling in the Development of Somites and Neural Crest
Paperback

The Role of Wnt Signalling in the Development of Somites and Neural Crest

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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.

1 Introduction 1. 1 Wnts and Development The f amily of Wnt genes consists of at least 19 members in vertebrates. Wnts ha v e multiple roles during normal development and aetiology of diseases (Wodarz and Nusse 1998; Moon et al. 2002, 2004). These genes encode for glycoproteins that are released in the intercellular space, acting as intercellular mediators (Moon et al. 1997). By binding to their special receptors, the Frizzled (Fz) receptors, they are able to activate at least three different pathways: the canonical, the non-canonical and the Ca 2+ pathway (Fig. 1 ). The Wnt family has been subdivided, using functional assays, into at least two subclasses. In Xenopus , Wnt1, Wnt3a and Wnt8 are able to induce axis duplication in embryos, whereas Wnt4, Wnt5a and Wnt11 cannot (Du et al. 1995). Those Wnts that are able to induce axis duplication are thought to act canonically; those who cannot are thought to act non-canonically. In the literature, therefore, some Wnts are called canonical Wnts while others are called n- cano nical Wnts, suggesting that a special Wnt always activates the same signalling pathway. It is unlikely that the specificity dictating cellular responses resides solely in the Wnt ligands because no one has reported sequence or structural motifs in Wnts that predict their activities in these cellular and embryonic assays.

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MORE INFO
Format
Paperback
Publisher
Springer-Verlag Berlin and Heidelberg GmbH & Co. KG
Country
Germany
Date
12 June 2008
Pages
64
ISBN
9783540777267

This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.

1 Introduction 1. 1 Wnts and Development The f amily of Wnt genes consists of at least 19 members in vertebrates. Wnts ha v e multiple roles during normal development and aetiology of diseases (Wodarz and Nusse 1998; Moon et al. 2002, 2004). These genes encode for glycoproteins that are released in the intercellular space, acting as intercellular mediators (Moon et al. 1997). By binding to their special receptors, the Frizzled (Fz) receptors, they are able to activate at least three different pathways: the canonical, the non-canonical and the Ca 2+ pathway (Fig. 1 ). The Wnt family has been subdivided, using functional assays, into at least two subclasses. In Xenopus , Wnt1, Wnt3a and Wnt8 are able to induce axis duplication in embryos, whereas Wnt4, Wnt5a and Wnt11 cannot (Du et al. 1995). Those Wnts that are able to induce axis duplication are thought to act canonically; those who cannot are thought to act non-canonically. In the literature, therefore, some Wnts are called canonical Wnts while others are called n- cano nical Wnts, suggesting that a special Wnt always activates the same signalling pathway. It is unlikely that the specificity dictating cellular responses resides solely in the Wnt ligands because no one has reported sequence or structural motifs in Wnts that predict their activities in these cellular and embryonic assays.

Read More
Format
Paperback
Publisher
Springer-Verlag Berlin and Heidelberg GmbH & Co. KG
Country
Germany
Date
12 June 2008
Pages
64
ISBN
9783540777267