We are analyzing https://link.springer.com/article/10.1186/s12915-017-0470-7.

Title:
PINK1 import regulation; a fine system to convey mitochondrial stress to the cytosol | BMC Biology
Description:
Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway.
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Keywords {🔍}

pink, pubmed, mitochondrial, article, google, scholar, cas, mitochondria, tom, complex, parkin, cleavage, central, import, omm, parl, kinase, proteins, activity, amino, activation, ubiquitin, domain, cell, membrane, mts, protease, mitophagy, fig, biol, acids, damaged, nterminal, cytosol, form, protein, recruitment, cleaved, degradation, localization, pathway, addition, kda, δψm, substrates, reported, tim, parlmediated, maaa, identified,

Topics {✒️}

parkinson's-disease-related kinase pink1 induce park2/parkin-mediated mitophagy n-end rule-dependent degradation n-terminally flag-tagged pink1 induce pink1/parkin-dependent mitophagy omm-accumulated full-length pink1 omm-localized full-length form hereditary early-onset parkinson' tom/tim23 super-complex formation article download pdf cells lacking pcp1p/ugo2p n-terminal tagging inhibits proof-reading-defective version n-end rule pathway stress-dependent import regulation n-terminal amino acid n-terminally tagged pink1 phos-tag western blotting n-terminal mts-deleted form phos-tag sds-page accumulated full-length pink1 imm-localized i-aaa protease mitochondrial ser/thr kinase mitochondrial-specific oxphos inhibitors ser/thr kinase domain sequence-specific intramembrane proteolysis helix confer cleavage-resistance dynamin-related gtpase involved pink1/parkin-dependent mitophagy bn-page analysis showed pink1/parkin-mediated mitophagy kinase activity-dependent manner pre-existing ubiquitin molecules parl-mediated intramembrane proteolysis stress-dependent pink1 accumulation n-terminally cleaved form productive tom/pink1 interactions tim23 complex-mediated import recent cryo-em analysis pink1-dependent ubiquitin phosphorylation conventional stop-transfer pathway membranes search search δotc-induced pink1 accumulation pcp1-mediated ccp1 cleavage omm-accumulated pink1 crosslinked parl-mediated pink1 cleavage pink1-parkin pathway activity pten-induced kinase-1 mitochondrial quality control autosomal recessive gene

Questions {❓}

As the Tim23 complex pulls the MTS into the matrix, what counteracts this and recognizes the OMS to promote retention of PINK1 in the OMM?
How does PINK1 accumulate on the OMM in response to mitochondrial damage?
PINK1, Parkin, and mitochondrial quality control: what can we learn about Parkinson's disease pathobiology?
Then how is full-length PINK1 laterally released from the TOM complex?
Why does PINK1 form a HMW complex with the TOM complex?

Schema {🗺️}

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         description:Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway.
         datePublished:2018-01-10T00:00:00Z
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            Parkin Recruitment
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      headline:PINK1 import regulation; a fine system to convey mitochondrial stress to the cytosol
      description:Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway.
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         PTEN-induced Putative Kinase 1 (PINK1)
         Healthy Mitochondrial Network
         Mitophagy
         PINK1 Mutant
         Parkin Recruitment
         Life Sciences
         general
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