Regulation of DNA repair by parkin

Kao, Shyan‐Yuan

doi:10.1016/j.bbrc.2009.03.048

Cited by 41 publications

(53 citation statements)

References 25 publications

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“…87 Parkin Was found to associate with PCNA in the nucleus and enhance NER-mediated resolution of UV-induced lesions and BER-mediated resolution of H 2 O 2 -induced lesion. 115,116 Recruited to damaged mitochondria (by PINK1) to promote their degradation through mitophagy. 29 …”

Section: E2f1mentioning

confidence: 99%

“…29,114 Deletion of parkin increases ROS generation due to accumulation of dysfunctional organelles, resulting in mtDNA and nDNA damage, which is the basis for parkin deficiency-associated Parkinson's disease. 115,116 In this sense, induction of autophagy has given promising results in mouse models of Alzheimer's disease 117 and other neurodegenerative diseases. 118 Further, the increased genomic instability observed in parkin-deleted cells could also be explained by the observation that parkin translocates from the cytosol to the nucleus where it participates in DDR after DNA damage.…”

Section: Parpmentioning

confidence: 99%

“…118 Further, the increased genomic instability observed in parkin-deleted cells could also be explained by the observation that parkin translocates from the cytosol to the nucleus where it participates in DDR after DNA damage. 115,116 Therefore, the parkin protein is an important factor in both DDR and autophagic removal of injured mitochondria.…”

Section: Parpmentioning

confidence: 99%

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Autophagy and genomic integrity

et al. 2013

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DNA lesions, constantly produced by endogenous and exogenous sources, activate the DNA damage response (DDR), which involves detection, signaling and repair of the damage. Autophagy, a lysosome-dependent degradation pathway that is activated by stressful situations such as starvation and oxidative stress, regulates cell fate after DNA damage and also has a pivotal role in the maintenance of nuclear and mitochondrial genomic integrity. Here, we review important evidence regarding the role played by autophagy in preventing genomic instability and tumorigenesis, as well as in micronuclei degradation. Several pathways governing autophagy activation after DNA injury and the influence of autophagy upon the processing of genomic lesions are also discussed herein. In this line, the mechanisms by which several proteins participate in both DDR and autophagy, and the importance of this crosstalk in cancer and neurodegeneration will be presented in an integrated fashion. At last, we present a hypothetical model of the role played by autophagy in dictating cell fate after genotoxic stress.

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Section: E2f1mentioning

confidence: 99%

Section: Parpmentioning

confidence: 99%

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Autophagy and genomic integrity

et al. 2013

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“…Mutation of parkin is one of the most prevalent causes of autosomal recessive familial PD and a recent study has shown that parkin is essential for optimal repair of DNA damage. Particularly, DNA damage induces nuclear translocation of parkin leading to interactions with PCNA and possibly other nuclear proteins involved in DNA repair (Kao, 2009). Moreover, parkin protects mitochondrial genome integrity and supports mitochondrial DNA (mtDNA) repair (Rothfuss et al, 2009).…”

Section: Polymorphisms Of Dna Repair Genes and Parkinson's Diseasementioning

confidence: 99%

“…It was shown that aprataxin participates in DNA repair suggesting that genes involved in DNA repair pathways might have a role in neurodegeneration (Hirano et al, 2007;Takahashi et al, 2007). Also parkin, encoded by one of the causative genes of Parkinson's disease (PD), seems to contribute to DNA repair (Kao, 2009). Variants and polymorphisms of DNA repair genes, particularly DNA base excision repair (BER) genes, have been investigated as possible risk factors for Alzheimer's disease (AD), Parkinson's disease, amyotrophic lateral sclerosis (ALS), and other neurodegenerative diseases (Coppedè & Migliore, 2010).…”

Section: Introductionmentioning

confidence: 99%

Variants and Polymorphisms of DNA Repair Genes and Neurodegenerative Diseases

Coppedè¹

2011

DNA Repair

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Role of Amyloidogenic and Non‐Amyloidogenic Protein Spaces in Neurodegenerative Diseases and their Mitigation Using Theranostic Agents

Suri,

Ramesh,

Bhandari

et al. 2024

ChemBioChem

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Neurodegenerative diseases (NDDs) refer to a complex heterogeneous group of diseases which are associated with the accumulation of amyloid fibrils or plaques in the brain leading to progressive loss of neuronal functions. Alzheimer’s disease is one of the major NDD responsible for 60‐80% of all dementia cases. Currently, there are no curative or disease‐reversing/modifying molecules for NDDs except a few such as donepezil, rivastigmine, galantamine, carbidopa and levodopa which treat the disease‐associated‐symptoms. Similarly, there are few FDA‐approved tracers such as flortaucipir for tau fibril‐imaging and florbetaben, flutemetamol, and florbetapir for amyloid‐imaging available for diagnosis. Recent advances in the cryo‐EM reported distinctly different microstructures for tau fibrils associated with different tauopathies highlighting the possibility to develop tauopathy‐specific imaging agents and therapeutics. In addition, it is important to identify the proteins that are associated with disease development and progression to know about their 3D structure to develop various diagnostics, therapeutics and theranostic agents. The current article discusses in detail the disease‐associated amyloid and non‐amyloid proteins along with their structural insights. We discuss various proteins associated with NDDs and their implications in NDD. In addition, we document chemical compounds developed for diagnosis and therapy of different NDDs with special emphasis on theranostic agents.

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Regulation of DNA repair by parkin

Cited by 41 publications

References 25 publications

Autophagy and genomic integrity

Autophagy and genomic integrity

Variants and Polymorphisms of DNA Repair Genes and Neurodegenerative Diseases

Role of Amyloidogenic and Non‐Amyloidogenic Protein Spaces in Neurodegenerative Diseases and their Mitigation Using Theranostic Agents

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