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SUMMARY:CANCELLED: Protein Intrinsic Disorder and Cell Signaling - A. Keit
 h Dunker\, Indiana University School of Medicine\, USA
DTSTART:20101001T151500Z
DTEND:20101001T160000Z
UID:TALK26099@talks.cam.ac.uk
CONTACT:Dr Madan Babu Mohan
DESCRIPTION:The standard view is that each protein’s amino acid sequence
  provides the information for it to fold into a specific 3D structure\, an
 d the active site formed within this structure enables function. Indeed\, 
 current biology and biochemical textbooks suggest that virtually all prote
 ins act via this sequence-to-structure-to-function paradigm. These views a
 re correct for enzymes\, which function as catalysts that accelerate chemi
 cal reactions. But a cell is not just an unregulated bag of enzyme-catalyz
 ed chemical reactions. Biological processes\, such as cell division\, deve
 lopment of different cell types\, etc. require a coordinated regulation an
 d organization of the various cellular components and compartments as well
  as regulation of the various chemical reactions. These regulatory functio
 ns involve proteins that interact with each other\, with nucleic acids\, a
 nd with a wide variety of other cellular components via complex networks. 
 These regulatory functions can also involve scaffolds and molecular machin
 es. We have used computational and bioinformatics methods to show that the
  regulatory signaling interactions in cells depend not only on protein 3D 
 structure\, but also depend on lack of 3D structure as well.  For signalin
 g proteins\, as well as for those involved in scaffolds and machines\, we 
 propose a new general paradigm\, given in short as sequence-to-flexible-en
 semble-to-function.  We will illustrate these ideas by providing a backgro
 und based on bioinformatics approaches and then by providing a number of s
 pecific\, well studied examples that directly illustrate the points being 
 made.   
LOCATION:Max Perutz Lecture Theatre\, MRC Laboratory of Molecular Biology\
 , Cambridge\, UK
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