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:20141216T084710Z
DTSTART:20150119T120000Z
SUMMARY:Cell Signaling by Extracellular Matrix Stiffness
UID:{http://www.columbasystems.com/customers/uom/gpp/eventid/}yr5-i3r0viw
 4-z81jxo
DESCRIPTION:Extracellular matrix (ECM) stiffness is transduced into cellu
 lar stiffness\, signaling\, and changes in cellular behavior. Integrins 
 and several of their associated focal adhesion proteins have been implic
 ated in sensing ECM stiffness. We investigated how an initial sensing ev
 ent is translated into cellular stiffness and a biologically interpretab
 le signal. We found that a pathway consisting of FAK\, Cas\, and Rac sel
 ectively transduced ECM stiffness into stable cellular stiffness\, incre
 ased abundance of cyclin D1\, and promoted S phase entry. Rac-dependent 
 intracellular stiffening involved its binding partner lamellipodin\, a p
 rotein that transmits Rac signals to the cytoskeleton during cell migrat
 ion. Our findings establish that mechanotransduction by a FAK-Cas-Rac-la
 mellipodin signaling module converts the external information encoded by
  ECM stiffness into stable cellular stiffness and mechanosensitive cell 
 cycling. 
STATUS:TENTATIVE
TRANSP:TRANSPARENT
CLASS:PUBLIC
LOCATION:B.4208\, Michael Smith Building\, Manchester
END:VEVENT
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