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SUMMARY:Aberrant Rho GTPase activation and signaling in cancer development
  - Channing Der - University of North Carolina at Chapel Hill\, NC
DTSTART:20081014T120000Z
DTEND:20081014T130000Z
UID:TALK13681@talks.cam.ac.uk
CONTACT:Luca Pellegrini
DESCRIPTION:Like the Ras oncogene proteins\, the Ras-related Rho family of
  small GTPases (20 human members) also function GDP/GTP-regulated binary s
 witches in cell surface receptor-stimulated signal transduction pathways t
 hat regulate actin cytoskeletal organization\, cell cycle progression\, an
 d gene expression.  Thus it is not surprising that like Ras\, considerable
  experimental analyses suggest that the aberrant activation of Rho GTPases
  can promote oncogenesis and cancer development.  However\, in contrast to
  Ras\, mutationally activated Rho GTPases have not been found in human can
 cers.  Instead\, the emerging picture is that Rho GTPases are activated in
  cancers by a diversity of indirect mechanisms.  For example\, Rho GTPases
  function as GDP/GTP-regulated binary switches that cycle between active G
 TP-bound and inactive GDP-bound states.  This cycle is controlled by both 
 positive (guanine nucleotide exchange factors\; RhoGEFs) and negative (GTP
 ase activating proteins\; RhoGAPs) regulatory proteins.  Thus\, it is the 
 inappropriate activation of RhoGEFs (e.g.\, Tiam1\, Asef\, TEM4) or loss o
 f function of RhoGAPs (e.g.\, DLC-1) that causes the indirect activation o
 f Rho GTPases in human cancers. Other mechanisms include aberrant gene exp
 ression (Rnd3/RhoE\, RhoGDI2\, P-Rex-1 and Ect2) or gene splicing (Rac1b).
   Similar mechanisms also deregulate Rho GTPases in other human diseases (
 neurological and developmental disorders). The different biochemical and m
 olecular mechanisms that cause aberrant Rho GTPase activation in human can
 cers will be presented. 
LOCATION:Lecture Theatre\, Biochemistry\, Department of (Sanger Building)
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