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Parkin-mediated responses against infection and wound involve TSPO-VDAC complex in Drosophila

Title
Parkin-mediated responses against infection and wound involve TSPO-VDAC complex in Drosophila
Authors
Cho, JH[Cho, Jae Ho]Park, JH[Park, Jeong Hyang]Chung, CG[Chung, Chang Geon]Shim, HJ[Shim, Hyun-Jung]Jeon, KH[Jeon, Keun Hye]Yu, SW[Yu, Seong-Woon]Lee, SB[Lee, Sung Bae]
DGIST Authors
Cho, JH[Cho, Jae Ho]; Park, JH[Park, Jeong Hyang]; Chung, CG[Chung, Chang Geon]; Shim, HJ[Shim, Hyun-Jung]; Jeon, KH[Jeon, Keun Hye]; Yu, SW[Yu, Seong-Woon]Lee, SB[Lee, Sung Bae]
Issue Date
2015-07-17
Citation
Biochemical and Biophysical Research Communications, 463(1-2), 1-6
Type
Article
Article Type
Article
Keywords
Amino Acid SequenceAnimal ExperimentAnimal ModelBacteria (Microorganisms)Bacterial InfectionBacterial LoadComparative StudyComplementary DnaControlled StudyDNA SynthesisDrosophilaGene InteractionHeterozygoteHomozygoteHypersensitivityImmune ResponseInnate Immune ResponseLoss of Function MutationNon-HumanParkinPriority JournalProteinQuantitative AnalysisReverse Transcriptase-Polymerase Chain ReactionRNARNA ExtractionSeptic InjurySequence HomologySurvival RateTranscription Factor GAL4TSPOTSPO ProteinTubulinUnclassified DrugVdac (Porin)Voltage Dependent Anion ChannelWoundWound Healing
ISSN
0006-291X
Abstract
Parkin, an E3 ubuquitin ligase associated with Parkinson's disease (PD), has recently been implicated in mediating innate immunity. However, molecular details regarding parkin-mediated immune response remain to be elucidated. Here, we identified mitochondrial TSPO-VDAC complex to genetically interact with parkin in mediating responses against infection and wound in Drosophila. The loss-of-function mutation in parkin results in defective immune response against bacterial infection. Additionally, parkin mutant larvae showed hypersensitivity against wound regardless of bacterial infection. Interestingly, the combinatorial trans-heterozygotic mutations in parkin and TSPO, or parkin and VDAC showed similar lethal tendency with parkin homozygous mutants. Furthermore, knockdown of TSPO alone also resulted in defective responses to infection and wound analogously to parkin mutants. Taken together, we propose that parkin cooperates with TSPO-VDAC complex to mediate responses against infection and wound. © 2015 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/20.500.11750/2877
DOI
10.1016/j.bbrc.2015.05.006
Publisher
Academic Press Inc.
Related Researcher
Files:
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Collection:
Brain and Cognitive SciencesLaboratory of Neuronal Cell Death1. Journal Articles


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