BEGIN:VCALENDAR
PRODID:-//Columba Systems Ltd//NONSGML CPNG/SpringViewer/ICal Output/3.3-
 M3//EN
VERSION:2.0
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VEVENT
DTSTAMP:20141106T160922Z
DTSTART:20141118T130000Z
DTEND:20141118T140000Z
SUMMARY:Molecular control of growth cone adhesion\, clutching and invasio
 n
UID:{http://www.columbasystems.com/customers/uom/gpp/eventid/}m62-i0pcd1t
 a-6bd55q
DESCRIPTION:This seminar is part of the Tissue Systems seminar series.   
                                                                         
                                                                         
                                                                         
  Growth cones of developing neurons are similar in many ways to migratin
 g fibroblasts\, patrolling immune cells\, and metastatic cancer cells.  
 Growth cones adhere to the extracellular matrix (ECM) through integrin r
 eceptors at sites termed point contacts.  Similar to fibroblast focal ad
 hesions\, point contacts dynamically link or “clutch” ECM proteins to th
 e actin cytoskeleton through a number of adaptor and signaling proteins.
  Like neutrophils\, growth cones are also guided by chemical gradients o
 f soluble and membrane-associated growth factors\, chemokines and guidan
 ce cues.  Interestingly\, we find that integrin adhesion is modulated by
  signals that occur downstream of growth factors and axon guidance cues\
 , suggesting that axon guidance may occur through regulation of integrin
  clutching.   Finally\, we have recently discovered that growth cones as
 semble actin-based protrusions that resemble cancer cell invadopodia. In
 vadopodia are basal or apical cell protrusions that target ECM degrading
  proteases to promote tissue invasion. We propose that growth cone invad
 osomes serve similar functions to allow axon guidance across the basal l
 amina or within tissues. 
STATUS:TENTATIVE
TRANSP:TRANSPARENT
CLASS:PUBLIC
LOCATION:Lecture Theatre\, Michael Smith Building\, Manchester
END:VEVENT
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