Erratum: Corrigendum: Sustained translational repression by eIF2α-P mediates prion neurodegeneration

Moreno, Julie A.; Radford, Helois; Peretti, Diego; Steinert, Joern R.; Verity, Nicholas; Martin, Maria Guerra; Halliday, Mark; Morgan, Jason; Dinsdale, David; Ortori, Catharine A.; Tsaytler, Pavel; Bertolotti, Anne; Willis, Anne E.; Bushell, Martin; Mallucci, Giovanna R.

doi:10.1038/nature13569

Cited by 1 publication

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“…Transgenic mice lacking a GD cause a sequential chain of PERK activation, which sustains the translational repression via eIF2α phosphorylation, and CHOP (Cyclophosphamide Hydroxydaunorubicin Oncovin Prednisone) upregulation and, ultimately, result in rapid neurodegeneration. 102,103 Similarly, during UPR activation, ATF6 is transferred to the Golgi apparatus and is split to create a highly active transcription factor related to the transcription of genes to participate in the canonical and noncanonical ERAD (endoplasmic-reticulum-associated protein degradation) system. Misfolded proteins are subject to UPS in the canonical ERAD system whereas the noncanonical ERAD system contributes to degradating aggregate-prone proteins through autophagy.…”

Section: ■ How Can Gut Microbiota Alternations Play a Role In Neurode...mentioning

confidence: 99%

“…A flexible N-terminal tail (FT) linked to a membrane-anchored globular domain (GD) has a great role in forming PrP C . Transgenic mice lacking a GD cause a sequential chain of PERK activation, which sustains the translational repression via eIF2α phosphorylation, and CHOP (Cyclophosphamide Hydroxydaunorubicin Oncovin Prednisone) upregulation and, ultimately, result in rapid neurodegeneration. , …”

Section: Role Of Molecular Disruptions In Neurodegenerative Diseasesmentioning

confidence: 99%

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Role of Polyphenols on Gut Microbiota and the Ubiquitin-Proteasome System in Neurodegenerative Diseases

Nargeh

Aliabadi

Ajami

2021

J. Agric. Food Chem.

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Today, neurodegenerative diseases have become a remarkable public health challenge due to their direct relation with aging. Accordingly, understanding the molecular and cellular mechanisms occurring in the pathogenesis of them is essential. Both protein aggregations as a result of the ubiquitin–proteasome system (UPS) inefficiency and gut microbiota alternation are the main pathogenic hallmarks. Polyphenols upregulating this system may decrease the developing rate of neurodegenerative diseases. Most of the dietary intake of polyphenols is converted into other microbial metabolites, which have completely different biological properties from the original polyphenols and should be thoroughly investigated. Herein, several prevalent neurodegenerative diseases are pinpointed to explain the role of gut microbiota alternations and the role of molecular changes, especially UPS down-regulation in their pathogenesis. Some of the most important polyphenols found in our diet are explained along with their microbial metabolites in the body.

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Section: ■ How Can Gut Microbiota Alternations Play a Role In Neurode...mentioning

confidence: 99%

Section: Role Of Molecular Disruptions In Neurodegenerative Diseasesmentioning

confidence: 99%

Role of Polyphenols on Gut Microbiota and the Ubiquitin-Proteasome System in Neurodegenerative Diseases

Nargeh

Aliabadi

Ajami

2021

J. Agric. Food Chem.

View full text Add to dashboard Cite

show abstract

Erratum: Corrigendum: Sustained translational repression by eIF2α-P mediates prion neurodegeneration

Cited by 1 publication

References 1 publication

Role of Polyphenols on Gut Microbiota and the Ubiquitin-Proteasome System in Neurodegenerative Diseases

Role of Polyphenols on Gut Microbiota and the Ubiquitin-Proteasome System in Neurodegenerative Diseases

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