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SUMMARY:ER stress and mitochondria  - Professor Giovanna Mallucci | Found
 ing Principal Investigator\, Altos Labs Cambridge Institute of Science\, C
 ambridge UK
DTSTART:20230301T150000Z
DTEND:20230301T160000Z
UID:TALK193783@talks.cam.ac.uk
CONTACT:Hannah Burns
DESCRIPTION:Widespread repression of protein synthesis rates is a key feat
 ure of Endoplasmic Reticulum (ER) stress\, mediated by the ER sensor kinas
 e PERK. This is a major mechanism of neuronal death in neurodegenerative d
 isease and a target for therapy. This talk will cover an overview of ER st
 ress in neurodegeneration and its modulation and also focus on new data fo
 cusing on the subcellular modulation of PERK activation.  Thus\, during E
 R stress\, while select transcripts escape this repression\, global transl
 ational down-regulation impacts crucial protein levels in all cellular com
 partments\, beyond the ER. How the cell manages this paradox is unclear. P
 ERK has a unique cytoplasmic loop within its kinase domain that binds PERK
 ’s target\, eIF2α. We identified the mitochondrial protein\, ATAD3A\, a
 s a new interactor of the loop\, binding to a highly conserved region with
 in it. During ER stress\, increased interaction between ATAD3A and PERK at
 tenuates PERK signalling to eIF2α\, removing the translational block on s
 everal mitochondrial proteins. This occurs at novel context-dependent\, mi
 tochondria-ER contact sites. The interaction provides a previously unknown
  mechanism for fine-tuning translational repression at a local level\, mit
 igating the impact of ER stress on mitochondria. Further\, it represents a
  new target for selective modulation of PERK-eIF2α signalling in diseases
  from cancer to neurodegeneration.
LOCATION:MRC MBU\, Level 7 Lecture Theatre\, The Keith Peters Building\, C
 B2 0XY
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