Journal Article (Review Article)

DZNE-2020-02785

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Parkin, PINK1 and mitochondrial integrity: emerging concepts of mitochondrial dysfunction in Parkinson's disease.

Pilsl, A. (First author)DZNE* ; Winklhofer, K. F. (Last author)DZNE*

2012
Springer Heidelberg

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Please use a persistent id in citations: doi:10.1007/s00401-011-0902-3

Abstract: Mitochondria are dynamic organelles which are essential for many cellular processes, such as ATP production by oxidative phosphorylation, lipid metabolism, assembly of iron sulfur clusters, regulation of calcium homeostasis, and cell death pathways. The dynamic changes in mitochondrial morphology, connectivity, and subcellular distribution are critically dependent on a highly regulated fusion and fission machinery. Mitochondrial function, dynamics, and quality control are vital for the maintenance of neuronal integrity. Indeed, there is mounting evidence that mitochondrial dysfunction plays a central role in several neurodegenerative diseases. In particular, the identification of genes linked to rare familial variants of Parkinson's disease has fueled research on mitochondrial aspects of the disease etiopathogenesis. Studies on the function of parkin and PINK1, which are associated with autosomal recessive parkinsonism, provided compelling evidence that these proteins can functionally interact to maintain mitochondrial integrity and to promote clearance of damaged and dysfunctional mitochondria. In this review we will summarize current knowledge about the impact of parkin and PINK1 on mitochondria.

Keyword(s): Animals (MeSH) ; Humans (MeSH) ; Mitochondrial Diseases: genetics (MeSH) ; Mitochondrial Diseases: metabolism (MeSH) ; Mitochondrial Diseases: physiopathology (MeSH) ; Mitochondrial Proteins: genetics (MeSH) ; Mitochondrial Proteins: physiology (MeSH) ; Parkinson Disease: genetics (MeSH) ; Parkinson Disease: metabolism (MeSH) ; Parkinson Disease: physiopathology (MeSH) ; Parkinsonian Disorders: genetics (MeSH) ; Parkinsonian Disorders: metabolism (MeSH) ; Parkinsonian Disorders: physiopathology (MeSH) ; Protein Kinases: genetics (MeSH) ; Protein Kinases: physiology (MeSH) ; Ubiquitin-Protein Ligases: genetics (MeSH) ; Ubiquitin-Protein Ligases: physiology (MeSH) ; Mitochondrial Proteins ; Ubiquitin-Protein Ligases ; parkin protein ; Protein Kinases ; PTEN-induced putative kinase

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Contributing Institute(s):

1. München common (München common)
2. Neurobiochemistry (AG Winklhofer)

Research Program(s):

1. 341 - Molecular Signaling (POF3-341) (POF3-341)

Appears in the scientific report 2012

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Database coverage:
; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF >= 15 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection

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