Rho in podosomes

Rho in podosomes

Integrins make a choice ignaling researchers have only a few factors with which to explain a whole lot of biology. On page 407, Goel et al. describe how two integrin variants channel the actions of a single factor, insulin-like growth factor (IGF), into two distinct pathways that induce either adhesion or proliferation. The ␤ 1A integrin variant was known to be associated with proliferation and...

Podosomes at a glance.

Cells can contact the extracellular matrix (ECM) through a variety of specialized structures. These cell-matrix contacts contain membrane proteins such as integrins, which bind both matrix components and cellular proteins, thus bridging the substratum and the cytoskeleton (reviewed in Adams, 2001). Matrix contacts provide the physical linkage that enables cells to adhere to and migrate on (or t...

Invasive podosomes and myoblast fusion.

p53 in cell invasion, podosomes, and invadopodia

Cell invasion of the extracellular matrix is prerequisite to cross tissue migration of tumor cells in cancer metastasis, and vascular smooth muscle cells in atherosclerosis. The tumor suppressor p53, better known for its roles in the regulation of cell cycle and apoptosis, has ignited much interest in its function as a suppressor of cell migration and invasion. How p53 and its gain-of-function ...

Active Rho is localized to podosomes induced by oncogenic Src and is required for their assembly and function

Transformation of fibroblasts by oncogenic Src causes disruption of actin stress fibers and formation of invasive adhesions called podosomes. Because the small GTPase Rho stimulates stress fiber formation, Rho inactivation by Src has been thought to be necessary for stress fiber disruption. However, we show here that Rho[GTP] levels do not decrease after transformation by activated Src. Inactiv...