Persistent ER stress causes GPI anchor deficit to convert a GPI-anchored prion protein into pro-PrP via the ATF6–miR449c-5p–PIGV axis

Li, Jing‐Feng; Li, S; Yu, Shengyou; Yang, Jie; Ke, Jing-Ru; Li, Huan; Chen, Heng; Lu, Mingjian; Sy, Man‐Sun; Gao, Zhao; Li, Chaoyang

doi:10.1016/j.jbc.2023.104982

Journal of Biological Chemistry

2023

DOI: 10.1016/j.jbc.2023.104982

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Persistent ER stress causes GPI anchor deficit to convert a GPI-anchored prion protein into pro-PrP via the ATF6–miR449c-5p–PIGV axis

Jing‐Feng Li

S Li

Shengyou Yu

et al.

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2024

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1-L Transcription in Prion Diseases

Nahalka

2024

IJMS

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Understanding the pathogenesis and mechanisms of prion diseases can significantly expand our knowledge in the field of neurodegenerative diseases. Prion biology is increasingly recognized as being relevant to the pathophysiology of Alzheimer’s disease and Parkinson’s disease, both of which affect millions of people each year. This bioinformatics study used a theoretical protein-RNA recognition code (1-L transcription) to reveal the post-transcriptional regulation of the prion protein (PrPC). The principle for this method is directly elucidated on PrPC, in which an octa-repeat can be 1-L transcribed into a GGA triplet repeat RNA aptamer known to reduce the misfolding of normal PrPC into abnormal PrPSc. The identified genes/proteins are associated with mitochondria, cancer, COVID-19 and ER-stress, and approximately half are directly or indirectly associated with prion diseases. For example, the octa-repeat supports CD44, and regions of the brain with astrocytic prion accumulation also display high levels of CD44.

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1-L Transcription in Prion Diseases

Nahalka

2024

IJMS

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Persistent ER stress causes GPI anchor deficit to convert a GPI-anchored prion protein into pro-PrP via the ATF6–miR449c-5p–PIGV axis

Cited by 1 publication

References 66 publications

1-L Transcription in Prion Diseases

1-L Transcription in Prion Diseases

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