001     139632
005     20240511120149.0
024 7 _ |a pmc:PMC7030885
|2 pmc
024 7 _ |a 10.1080/19336896.2017.1356559
|2 doi
024 7 _ |a pmid:28956717
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024 7 _ |a 1933-6896
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024 7 _ |a 1933-690X
|2 ISSN
024 7 _ |a altmetric:26740627
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037 _ _ |a DZNE-2020-05954
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Lechler, Marie C
|0 P:(DE-2719)2810617
|b 0
|e First author
|u dzne
245 _ _ |a More stressed out with age? Check your RNA granule aggregation.
260 _ _ |a London [u.a.]
|c 2017
|b Taylor & Francis
264 _ 1 |3 online
|2 Crossref
|b Informa UK Limited
|c 2017-10-12
264 _ 1 |3 print
|2 Crossref
|b Informa UK Limited
|c 2017-09-03
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1715347867_4832
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Low complexity (LC) prion-like domains are over-represented among RNA-binding proteins (RBPs) and contribute to the dynamic nature of RNA granules. Importantly, several neurodegenerative diseases are characterized by cytoplasmic 'solid' aggregates formed by mainly nuclear RBPs harboring LC prion-like domains. Although RBP aggregation in disease has been extensively characterized, it remains unknown how the process of aging disturbs RBP dynamics. Our recent study revealed that RNA granule components including 2 key stress granule RBPs with LC prion-like domains, PAB-1 and TIAR-2, aggregate in aged Caenorhabditis elegans in the absence of disease. Here we present new evidence showing that sustained stress granule formation triggers RBP aggregation. In addition, we demonstrate that mild chronic stress during aging promotes mislocalization of nuclear RBPs. We discuss the consequences of aberrant interactions between age-related RBP aggregation and disease-associated RBP aggregation. In particular, we show that FUST-1 and PAB-1 co-localize in aberrant cytoplasmic accumulations. Significantly, long-lived animals with reduced insulin/IGF-1 signaling abrogate stress granule RBP aggregation through activation of the transcription factors HSF-1 and DAF-16. We evaluate the different mechanisms that could maintain dynamic stress granules. Together these findings highlight how changes with age could contribute to pathogenesis in neurodegenerative diseases and disruption of RNA homeostasis.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Caenorhabditis elegans Proteins
|2 NLM Chemicals
650 _ 7 |a Forkhead Transcription Factors
|2 NLM Chemicals
650 _ 7 |a Poly(A)-Binding Protein I
|2 NLM Chemicals
650 _ 7 |a Prions
|2 NLM Chemicals
650 _ 7 |a Proteome
|2 NLM Chemicals
650 _ 7 |a RNA-Binding Proteins
|2 NLM Chemicals
650 _ 7 |a Transcription Factors
|2 NLM Chemicals
650 _ 7 |a daf-16 protein, C elegans
|2 NLM Chemicals
650 _ 7 |a heat shock factor-1, C elegans
|2 NLM Chemicals
650 _ 7 |a RNA
|0 63231-63-0
|2 NLM Chemicals
650 _ 2 |a Aging: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Caenorhabditis elegans: genetics
|2 MeSH
650 _ 2 |a Caenorhabditis elegans Proteins: metabolism
|2 MeSH
650 _ 2 |a Cytoplasmic Granules: metabolism
|2 MeSH
650 _ 2 |a Forkhead Transcription Factors: metabolism
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Longevity
|2 MeSH
650 _ 2 |a Neurodegenerative Diseases: metabolism
|2 MeSH
650 _ 2 |a Poly(A)-Binding Protein I: metabolism
|2 MeSH
650 _ 2 |a Prions: metabolism
|2 MeSH
650 _ 2 |a Protein Aggregation, Pathological: metabolism
|2 MeSH
650 _ 2 |a Proteome: chemistry
|2 MeSH
650 _ 2 |a RNA: metabolism
|2 MeSH
650 _ 2 |a RNA-Binding Proteins: metabolism
|2 MeSH
650 _ 2 |a Stress, Physiological
|2 MeSH
650 _ 2 |a Transcription Factors: metabolism
|2 MeSH
700 1 _ |a David, Della C
|0 P:(DE-2719)2810353
|b 1
|e Last author
|u dzne
773 1 8 |a 10.1080/19336896.2017.1356559
|b : Informa UK Limited, 2017-09-03
|n 5
|p 313-322
|3 journal-article
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|t Prion
|v 11
|y 2017
|x 1933-6896
773 _ _ |a 10.1080/19336896.2017.1356559
|g Vol. 11, no. 5, p. 313 - 322
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|q 11:5<313 - 322
|p 313-322
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856 4 _ |y OpenAccess
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856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 1
|6 P:(DE-2719)2810353
913 1 _ |a DE-HGF
|b Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-342
|3 G:(DE-HGF)POF3
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914 1 _ |y 2017
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21