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Wnt/frizzled signaling in mammalian ...

Castelo-Soccio, Leslie A.

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Wnt/frizzled signaling in mammalian cell culture and mouse mammary tissue.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Wnt/frizzled signaling in mammalian cell culture and mouse mammary tissue./
Author:	Castelo-Soccio, Leslie A.
Description:	162 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2236.
Contained By:	Dissertation Abstracts International65-05B.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3134717
ISBN:	0496819437

Wnt/frizzled signaling in mammalian cell culture and mouse mammary tissue.
Castelo-Soccio, Leslie A.

Wnt/frizzled signaling in mammalian cell culture and mouse mammary tissue. - 162 p.

Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2236.

Thesis (Ph.D.)--Weill Medical College of Cornell University, 2004.

Writ proteins, a family of 19 cysteine-rich extracellular signaling molecules, act through beta-catenin-dependent and independent pathways by binding LRP5/6 and/or Frizzled proteins on the cell surface. Previously, Wnt proteins were categorized by their ability to signal through beta-catenin. However, we found that Wnt4 cannot be classified in this manner because it stimulates canonical/beta-catenin signaling in some cell lines (10T½) but induces non-canonical/c-Jun phosphorylation in others (3T3). We hypothesized that distinct cellular responses to Wnt4 reflect differential expression and abundance of particular Writ receptors on the cell surface. Overexpression of Frizzled 5 or Frizzled 9 but not other Frizzleds, enabled Wnt4 to activate beta-catenin signaling, suggesting that receptor expression and abundance may be mediating canonical versus non-canonical signaling. In cells in which Wnt4 does not activate canonical signaling, it mediates a novel c-Jun phosphorylation response. 3T3 cells show three distinct responses to Writ proteins: Dvl phosphorylation occurs in response to Wnt1, Wnt4 and Wnt5a, but beta-catenin stabilization and c-Jun phosphorylation only occur in response to Wnt1 or Wnt4, respectively. Overall, these cell studies of Writ signaling suggest that Writs can only be classified as canonical or non-canonical within the confines of a given cell context.

ISBN: 0496819437Subjects--Topical Terms:

1017719
Biology, Molecular.

Wnt/frizzled signaling in mammalian cell culture and mouse mammary tissue.
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245 1 0 $a Wnt/frizzled signaling in mammalian cell culture and mouse mammary tissue.
300 $a 162 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-05, Section: B, page: 2236.
500 $a Adviser: Anthony M. C. Brown.
502 $a Thesis (Ph.D.)--Weill Medical College of Cornell University, 2004.
520 $a Writ proteins, a family of 19 cysteine-rich extracellular signaling molecules, act through beta-catenin-dependent and independent pathways by binding LRP5/6 and/or Frizzled proteins on the cell surface. Previously, Wnt proteins were categorized by their ability to signal through beta-catenin. However, we found that Wnt4 cannot be classified in this manner because it stimulates canonical/beta-catenin signaling in some cell lines (10T½) but induces non-canonical/c-Jun phosphorylation in others (3T3). We hypothesized that distinct cellular responses to Wnt4 reflect differential expression and abundance of particular Writ receptors on the cell surface. Overexpression of Frizzled 5 or Frizzled 9 but not other Frizzleds, enabled Wnt4 to activate beta-catenin signaling, suggesting that receptor expression and abundance may be mediating canonical versus non-canonical signaling. In cells in which Wnt4 does not activate canonical signaling, it mediates a novel c-Jun phosphorylation response. 3T3 cells show three distinct responses to Writ proteins: Dvl phosphorylation occurs in response to Wnt1, Wnt4 and Wnt5a, but beta-catenin stabilization and c-Jun phosphorylation only occur in response to Wnt1 or Wnt4, respectively. Overall, these cell studies of Writ signaling suggest that Writs can only be classified as canonical or non-canonical within the confines of a given cell context.
520 $a Constitutive activation of Writ signaling leads to tumorigenesis, as ectopic expression of Wnt1 in mouse mammary tissue leads to alveolar hyperplasia and tumors. We generated transgenic mice expressing in the mammary gland an inhibitory form of the Wnt receptor Frizzled 8 (ExFz8). A significant reduction in ductal outgrowth was observed at 9 weeks in multiple transgenic strains compared to wildtype, though this reduction was not seen at 6 weeks and normal ductal growth was restored by 12 weeks. Finally, in Wnt1/ExFz8 bitransgenic mice, ExFz8 decreased hyperplasia and markedly inhibited tumorigenesis by Wnt1.
590 $a School code: 0967.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Genetics. $3 1017730
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710 2 0 $a Weill Medical College of Cornell University. $3 1021736
773 0 $t Dissertation Abstracts International $g 65-05B.
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790 $a 0967
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3134717