QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online March 2, 2004
doi: 10.1242/10.1242/jcs.01111

This Article Summary Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Frame, M. C. Search for Related Content PubMed PubMed Citation Articles by Frame, M. C. Social Bookmarking                         What's this?

Newest findings on the oldest oncogene; how activated src does it

Cancer Research UK Beatson Laboratories, Garscube Estate, Switchback Road, Bearsden, Glasgow, G61 1BD, UK

View larger version (53K): [in a new window]   Fig. 1. v-Src, or activated Src527F, induces tyrosine phosphorylation of cell-cell adherens junction components (the cadherin/catenin system), or acts by phosphorylating protein regulators of adherens junctions, such as Hakai, to cause disruption, or weakening, of cell-cell adhesions. Internalised cadherin molecules and released binding proteins are indicated. In a somewhat analogous manner, oncogenic Src weakens the links between cell-matrix adhesions and the actin cytoskeleton in the cell interior, in some situations by causing phosphorylation of the integrin cytoplasmic tails, but also by phosphorylating R-Ras and causing a change in integrin activation status.

View larger version (57K): [in a new window]   Fig. 2. Some of the major v-Src effector pathways (discussed in the text) that control and co-ordinate key cellular responses, including growth and survival, adhesion/actin dynamics, matrix-degrading enzyme production and invasion. This does not represent an exhaustive list of v-Src activities in transformed cells.

View larger version (70K): [in a new window]   Fig. 3. Epithelial cells that are held together by intercellular contacts (top-left), and shown for cells from the KM12C colon cancer cell series (visualized by immunofluorescence) (top right), become dispersed as a consequence of expression of Src527F (bottom-left), shown for KM12C cells (bottom-right). As described in the text, cadherin-dependent cell-cell contacts are lost and assembly of integrin-associated adhesions are enhanced as a result of oncogenic Src, resulting in the `adhesion switch' phenotype associated with acquisition of a more mesenchymal-like morphology. Cells in the top-right and bottom-right panels are stained with anti-E-cadherin and anti-vinculin, respectively. Images are courtesy of Egle Avizienyte.

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

Twitter