Phosphatases of α-synuclein, LRRK2, and tau: important players in the phosphorylation-dependent pathology of Parkinsonism
Identifieur interne : 000880 ( Main/Exploration ); précédent : 000879; suivant : 000881Phosphatases of α-synuclein, LRRK2, and tau: important players in the phosphorylation-dependent pathology of Parkinsonism
Auteurs : Jean-Marc Taymans ; Veerle BaekelandtSource :
- Frontiers in Genetics [ 1664-8021 ] ; 2014.
Abstract
An important challenge in the field of Parkinson’s disease (PD) is to develop disease modifying therapies capable of stalling or even halting disease progression. Coupled to this challenge is the need to identify disease biomarkers, in order to identify pre-symptomatic hallmarks of disease and monitor disease progression. The answer to these challenges lies in the elucidation of the molecular causes underlying PD, for which important leads are disease genes identified in studies investigating the underlying genetic causes of PD. LRRK2 and α-syn have been both linked to familial forms of PD as well as associated to sporadic PD. Another gene, microtubule associated protein tau (MAPT), has been genetically linked to a dominant form of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) and genome-wide association studies report a strong association between MAPT and sporadic PD. Interestingly, LRRK2, α-syn, and tau are all phosphorylated proteins, and their phosphorylation patterns are linked to disease. In this review, we provide an overview of the evidence linking LRRK2, α-syn, and tau phosphorylation to PD pathology and focus on studies which have identified phosphatases responsible for dephosphorylation of pathology-related phosphorylations. We also discuss how the LRRK2, α-syn, and tau phosphatases may point to separate or cross-talking pathological pathways in PD. Finally, we will discuss how the study of phosphatases of dominant Parkinsonism proteins opens perspectives for targeting pathological phosphorylation events.
Url:
DOI: 10.3389/fgene.2014.00382
PubMed: 25426138
PubMed Central: 4224088
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Phosphatases of α-synuclein, LRRK2, and tau: important players in the phosphorylation-dependent pathology of Parkinsonism</title><author><name sortKey="Taymans, Jean Marc" sort="Taymans, Jean Marc" uniqKey="Taymans J" first="Jean-Marc" last="Taymans">Jean-Marc Taymans</name></author><author><name sortKey="Baekelandt, Veerle" sort="Baekelandt, Veerle" uniqKey="Baekelandt V" first="Veerle" last="Baekelandt">Veerle Baekelandt</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25426138</idno><idno type="pmc">4224088</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4224088</idno><idno type="RBID">PMC:4224088</idno><idno type="doi">10.3389/fgene.2014.00382</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000934</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000934</idno><idno type="wicri:Area/Pmc/Curation">000930</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000930</idno><idno type="wicri:Area/Pmc/Checkpoint">000311</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000311</idno><idno type="wicri:Area/Ncbi/Merge">001579</idno><idno type="wicri:Area/Ncbi/Curation">001579</idno><idno type="wicri:Area/Ncbi/Checkpoint">001579</idno><idno type="wicri:Area/Main/Merge">000885</idno><idno type="wicri:Area/Main/Curation">000880</idno><idno type="wicri:Area/Main/Exploration">000880</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Phosphatases of α-synuclein, LRRK2, and tau: important players in the phosphorylation-dependent pathology of Parkinsonism</title><author><name sortKey="Taymans, Jean Marc" sort="Taymans, Jean Marc" uniqKey="Taymans J" first="Jean-Marc" last="Taymans">Jean-Marc Taymans</name></author><author><name sortKey="Baekelandt, Veerle" sort="Baekelandt, Veerle" uniqKey="Baekelandt V" first="Veerle" last="Baekelandt">Veerle Baekelandt</name></author></analytic><series><title level="j">Frontiers in Genetics</title><idno type="eISSN">1664-8021</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>An important challenge in the field of Parkinson’s disease (PD) is to develop disease modifying therapies capable of stalling or even halting disease progression. Coupled to this challenge is the need to identify disease biomarkers, in order to identify pre-symptomatic hallmarks of disease and monitor disease progression. The answer to these challenges lies in the elucidation of the molecular causes underlying PD, for which important leads are disease genes identified in studies investigating the underlying genetic causes of PD. LRRK2 and α-syn have been both linked to familial forms of PD as well as associated to sporadic PD. Another gene, microtubule associated protein tau (MAPT), has been genetically linked to a dominant form of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) and genome-wide association studies report a strong association between MAPT and sporadic PD. Interestingly, LRRK2, α-syn, and tau are all phosphorylated proteins, and their phosphorylation patterns are linked to disease. In this review, we provide an overview of the evidence linking LRRK2, α-syn, and tau phosphorylation to PD pathology and focus on studies which have identified phosphatases responsible for dephosphorylation of pathology-related phosphorylations. We also discuss how the LRRK2, α-syn, and tau phosphatases may point to separate or cross-talking pathological pathways in PD. Finally, we will discuss how the study of phosphatases of dominant Parkinsonism proteins opens perspectives for targeting pathological phosphorylation events.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Anderson, J P" uniqKey="Anderson J">J. P. Anderson</name></author><author><name sortKey="Walker, D E" uniqKey="Walker D">D. E. Walker</name></author><author><name sortKey="Goldstein, J M" uniqKey="Goldstein J">J. M. Goldstein</name></author><author><name sortKey="De Laat, R" uniqKey="De Laat R">R. 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Lincoln</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Baekelandt, Veerle" sort="Baekelandt, Veerle" uniqKey="Baekelandt V" first="Veerle" last="Baekelandt">Veerle Baekelandt</name><name sortKey="Taymans, Jean Marc" sort="Taymans, Jean Marc" uniqKey="Taymans J" first="Jean-Marc" last="Taymans">Jean-Marc Taymans</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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