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000137919 0247_ $$2doi$$a10.1172/JCI79300
000137919 0247_ $$2pmid$$apmid:25822020
000137919 0247_ $$2pmc$$apmc:PMC4611569
000137919 0247_ $$2ISSN$$a0021-9738
000137919 0247_ $$2ISSN$$a1558-8238
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000137919 037__ $$aDZNE-2020-04241
000137919 041__ $$aEnglish
000137919 082__ $$a610
000137919 1001_ $$aMeka, Durga Praveen$$b0
000137919 245__ $$aParkin cooperates with GDNF/RET signaling to prevent dopaminergic neuron degeneration.
000137919 260__ $$aAnn Arbor, Mich.$$bASCJ$$c2015
000137919 264_1 $$2Crossref$$3online$$bAmerican Society for Clinical Investigation$$c2015-03-30
000137919 264_1 $$2Crossref$$3print$$bAmerican Society for Clinical Investigation$$c2015-05-01
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000137919 520__ $$aParkin and the glial cell line-derived neurotrophic factor (GDNF) receptor RET have both been independently linked to the dopaminergic neuron degeneration that underlies Parkinson's disease (PD). In the present study, we demonstrate that there is genetic crosstalk between parkin and the receptor tyrosine kinase RET in two different mouse models of PD. Mice lacking both parkin and RET exhibited accelerated dopaminergic cell and axonal loss compared with parkin-deficient animals, which showed none, and RET-deficient mice, in which we found moderate degeneration. Transgenic expression of parkin protected the dopaminergic systems of aged RET-deficient mice. Downregulation of either parkin or RET in neuronal cells impaired mitochondrial function and morphology. Parkin expression restored mitochondrial function in GDNF/RET-deficient cells, while GDNF stimulation rescued mitochondrial defects in parkin-deficient cells. In both cases, improved mitochondrial function was the result of activation of the prosurvival NF-κB pathway, which was mediated by RET through the phosphoinositide-3-kinase (PI3K) pathway. Taken together, these observations indicate that parkin and the RET signaling cascade converge to control mitochondrial integrity and thereby properly maintain substantia nigra pars compacta dopaminergic neurons and their innervation in the striatum. The demonstration of crosstalk between parkin and RET highlights the interplay in the protein network that is altered in PD and suggests potential therapeutic targets and strategies to treat PD.
000137919 536__ $$0G:(DE-HGF)POF3-341$$a341 - Molecular Signaling (POF3-341)$$cPOF3-341$$fPOF III$$x0
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000137919 650_7 $$2NLM Chemicals$$aGdnf protein, mouse
000137919 650_7 $$2NLM Chemicals$$aGlial Cell Line-Derived Neurotrophic Factor
000137919 650_7 $$2NLM Chemicals$$aNF-kappa B
000137919 650_7 $$2NLM Chemicals$$aRecombinant Fusion Proteins
000137919 650_7 $$08L70Q75FXE$$2NLM Chemicals$$aAdenosine Triphosphate
000137919 650_7 $$0EC 2.3.2.27$$2NLM Chemicals$$aUbiquitin-Protein Ligases
000137919 650_7 $$0EC 2.3.2.27$$2NLM Chemicals$$aparkin protein
000137919 650_7 $$0EC 2.7.1.-$$2NLM Chemicals$$aPhosphatidylinositol 3-Kinases
000137919 650_7 $$0EC 2.7.10.1$$2NLM Chemicals$$aProto-Oncogene Proteins c-ret
000137919 650_7 $$0EC 2.7.10.1$$2NLM Chemicals$$aRet protein, mouse
000137919 650_2 $$2MeSH$$aAdenosine Triphosphate: biosynthesis
000137919 650_2 $$2MeSH$$aAnimals
000137919 650_2 $$2MeSH$$aAnxiety: genetics
000137919 650_2 $$2MeSH$$aCell Line
000137919 650_2 $$2MeSH$$aCell Size
000137919 650_2 $$2MeSH$$aDisease Progression
000137919 650_2 $$2MeSH$$aDopaminergic Neurons: pathology
000137919 650_2 $$2MeSH$$aExploratory Behavior
000137919 650_2 $$2MeSH$$aGlial Cell Line-Derived Neurotrophic Factor: deficiency
000137919 650_2 $$2MeSH$$aGlial Cell Line-Derived Neurotrophic Factor: genetics
000137919 650_2 $$2MeSH$$aGlial Cell Line-Derived Neurotrophic Factor: physiology
000137919 650_2 $$2MeSH$$aMice
000137919 650_2 $$2MeSH$$aMice, Knockout
000137919 650_2 $$2MeSH$$aMice, Transgenic
000137919 650_2 $$2MeSH$$aMitochondria: pathology
000137919 650_2 $$2MeSH$$aNF-kappa B: physiology
000137919 650_2 $$2MeSH$$aNerve Degeneration: pathology
000137919 650_2 $$2MeSH$$aParkinsonian Disorders: genetics
000137919 650_2 $$2MeSH$$aParkinsonian Disorders: pathology
000137919 650_2 $$2MeSH$$aPhosphatidylinositol 3-Kinases: physiology
000137919 650_2 $$2MeSH$$aProto-Oncogene Proteins c-ret: deficiency
000137919 650_2 $$2MeSH$$aProto-Oncogene Proteins c-ret: genetics
000137919 650_2 $$2MeSH$$aProto-Oncogene Proteins c-ret: physiology
000137919 650_2 $$2MeSH$$aRecombinant Fusion Proteins: metabolism
000137919 650_2 $$2MeSH$$aRotarod Performance Test
000137919 650_2 $$2MeSH$$aSignal Transduction
000137919 650_2 $$2MeSH$$aSubstantia Nigra: pathology
000137919 650_2 $$2MeSH$$aUbiquitin-Protein Ligases: deficiency
000137919 650_2 $$2MeSH$$aUbiquitin-Protein Ligases: genetics
000137919 650_2 $$2MeSH$$aUbiquitin-Protein Ligases: physiology
000137919 7001_ $$0P:(DE-2719)9000425$$aMüller-Rischart, Anne Kathrin$$b1$$udzne
000137919 7001_ $$aNidadavolu, Prakash$$b2
000137919 7001_ $$aMohammadi, Behnam$$b3
000137919 7001_ $$aMotori, Elisa$$b4
000137919 7001_ $$aPonna, Srinivas Kumar$$b5
000137919 7001_ $$0P:(DE-HGF)0$$aAboutalebi, Helia$$b6
000137919 7001_ $$0P:(DE-HGF)0$$aBassal, Mahmoud$$b7
000137919 7001_ $$aAnnamneedi, Anil$$b8
000137919 7001_ $$aFinckh, Barbara$$b9
000137919 7001_ $$0P:(DE-HGF)0$$aMiesbauer, Margit$$b10
000137919 7001_ $$aRotermund, Natalie$$b11
000137919 7001_ $$aLohr, Christian$$b12
000137919 7001_ $$0P:(DE-HGF)0$$aTatzelt, Jörg$$b13
000137919 7001_ $$0P:(DE-2719)9000369$$aWinklhofer, Konstanze F$$b14$$udzne
000137919 7001_ $$0P:(DE-HGF)0$$aKramer, Edgar R$$b15$$eCorresponding author
000137919 77318 $$2Crossref$$3journal-article$$a10.1172/jci79300$$b : American Society for Clinical Investigation, 2015-03-30$$n5$$p1873-1885$$tJournal of Clinical Investigation$$v125$$x0021-9738$$y2015
000137919 773__ $$0PERI:(DE-600)2018375-6$$a10.1172/JCI79300$$gVol. 125, no. 5, p. 1873 - 1885$$n5$$p1873-1885$$q125:5<1873 - 1885$$tThe journal of clinical investigation$$v125$$x0021-9738$$y2015
000137919 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4611569
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