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SUMMARY:Selective autophagy: when being picky pays of - Ana-Maria Cuervo\,
  Albert Einstein College of Medicine 
DTSTART:20130502T151500Z
DTEND:20130502T170000Z
UID:TALK43663@talks.cam.ac.uk
CONTACT:Scientific Meetings Co-ordinator
DESCRIPTION:All types of autophagy fulfill two important functions in mamm
 alian cells\, serving both as an alternative source of energy\, when nutri
 ents are scarce\, and as an efficient mechanism for the removal of any int
 racellular damaged structures. In this talk\, I will focus on a selective 
 form of autophagy\, known as chaperone-mediated autophagy (CMA) and the co
 nnections between this pathway and cellular quality control. \nCMA mediate
 s selective targeting of soluble cytosolic proteins to lysosomes for their
  degradation. CMA is active in most cell types in mammalians but its activ
 ity varies depending on cellular conditions. Maximal activation of this pa
 thway occurs during stress or in conditions leading to increased amount of
  misfolded/damaged proteins. Degradation via this pathway requires a set o
 f cytosolic and lysosomal chaperones and a receptor protein at the lysosom
 al membrane\, the lysosome-associated membrane protein type 2A (LAMP-2A). 
 The limiting step of this type of autophagy is the binding of substrates t
 o LAMP-2A. We have found that changes in the levels and organization of LA
 MP-2A at the lysosomal membrane underlie the molecular basis for the regul
 ation of CMA. Two lysosomal chaperones\, hsc70 and hsp90\, are critical re
 gulators of the higher order organization of LAMP-2A and the assembly of t
 he translocation complex.\n. In recent years\, the better molecular charac
 terization of CMA has considerably advanced our understanding of the physi
 ological role of this pathway and the consequences of its malfunctioning i
 n the pathogenesis of detrimental human pathologies\, such as cancer\, neu
 rodegenerative and metabolic diseases. \n    In this talk\, I will describ
 e some of the recent findings on the interplay between pathogenic proteins
  and CMA. We are addressing this interaction as a two-side relationship: 1
 ) the contribution of CMA to the removal of pathogenic proteins and 2) the
  effect that pathogenic proteins can exert on CMA activity. Lastly\, I wil
 l comment on the functional decline of CMA with age and the reasons behind
  this decline. \n
LOCATION:Max Perutz Lecture Theatre\, Medical Research Council (MRC) (MRC 
 Laboratory of Molecular Biol
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