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SUMMARY:Linking dynamic signaling events within the same cell - John Albec
 k (University of California\, Davis)
DTSTART:20160405T130000Z
DTEND:20160405T134500Z
UID:TALK65320@talks.cam.ac.uk
CONTACT:INI IT
DESCRIPTION:In intracellular signaling pathways\, biochemical activation e
 vents are transmitted from one node within the signaling network to anothe
 r.&nbsp\; Recent work examining the information capacity of signaling path
 ways has concluded that most signaling pathways have limited abilities to 
 resolve different strengths of inputs.&nbsp\; However\, these studies are 
 based on data in which only a single signal is measured in each cell\, in 
 response to a given cell\, with the limitation that transmission of a sign
 al from one signaling node to another cannot be directly observed.&nbsp\; 
 Other published data suggest that single cells may have a much higher capa
 city to transmit quantitative information\, which is obscured by populatio
 n heterogeneity.&nbsp\; To better understand the properties of information
  transmission through biochemical cascades in individual cells\, we have d
 eveloped a panel of live-cell reporters to monitor multiple signaling even
 ts in the cell proliferation and growth network (CPGN).&nbsp\; These repor
 ters include activity biosensors for the kinases ERK\, Akt\, mTOR\, and AM
 PK\, and CRISPR-based reporters for ERK target gene expression.&nbsp\; Exp
 erimental analysis with these tools reveals the temporal and quantitative 
 linkage properties between nodes of the CPGN.&nbsp\; I will discuss two st
 udies currently underway in our lab.&nbsp\; The first examines the how the
  CPGN manages the interplay between ATP-producing and ATP-consuming proces
 ses during cell proliferation\; we find that loss of Akt signaling results
  in unstable levels of ATP and NADH in proliferating cells.&nbsp\; The sec
 ond project focuses on how variations in amplitude and duration of ERK act
 ivity control the expression of the target gene Fra-1\, which is involved 
 in metastasis\; here\, we show that cancer therapeutics directed at inhibi
 ting this pathway create strikingly different kinetics of ERK activity at 
 the single-cell level\, with distinct effects on Fra-1 expression. <br><br
 ><br><br>
LOCATION:Seminar Room 1\, Newton Institute
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