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News & Views

Parkin‐independent mitophagy—FKBP8 takes the stage

Grace GY Lim, Kah‐Leong Lim
DOI 10.15252/embr.201744313 | Published online 17.05.2017
EMBO reports (2017) e201744313
Grace GY Lim
Neurodegeneration Research Laboratory, National Neuroscience Institute, Singapore City, Singapore
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Kah‐Leong Lim
Neurodegeneration Research Laboratory, National Neuroscience Institute, Singapore City, SingaporeDepartment of Physiology, National University of Singapore, Singapore City, SingaporeDuke‐NUS Medical School, Singapore City, Singapore
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Author Affiliations

  1. Grace GY Lim1 and
  2. Kah‐Leong Lim (Kah_Leong_Lim{at}nni.com.sg)1,2,3
  1. 1Neurodegeneration Research Laboratory, National Neuroscience Institute, Singapore City, Singapore
  2. 2Department of Physiology, National University of Singapore, Singapore City, Singapore
  3. 3Duke‐NUS Medical School, Singapore City, Singapore
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Abstract

Although the Parkin/PINK1 pathway has received considerable attention in recent years as a key regulator of mitophagy in mammals, it is important to recognize that multiple mitophagy receptors like BNIP3, NIX, and FUNDC1 exist that can promote the selective clearance of mitochondria in the absence of Parkin. In this issue, Bhujabal et al expand the repertoire of Parkin‐independent mitophagy receptors to include the anti‐apoptotic protein, FKBP8. The authors demonstrate that FKBP8 interacts preferentially with LC3A via its LIR motif to destroy damaged mitochondria. During the process, FKBP8 escapes from the destruction presumably to prevent apoptosis during mitophagy [1].

See also Z Bhujabal et al (June 2017)

  • © 2017 The Authors
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In this Issue
Volume 19, Issue 4
01 April 2018 | pp -
EMBO reports: 19 (4)
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