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Miao Yang

Researcher at University of South Australia

Publications -  15
Citations -  547

Miao Yang is an academic researcher from University of South Australia. The author has contributed to research in topics: Amyloid beta & Amyloid precursor protein. The author has an hindex of 12, co-authored 15 publications receiving 474 citations. Previous affiliations of Miao Yang include Flinders University.

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Journal ArticleDOI

p75NTR Regulates Aβ Deposition by Increasing Aβ Production But Inhibiting Aβ Aggregation with Its Extracellular Domain

TL;DR: The data suggest that p75NTR plays a critical role in regulating Aβ levels by both increasing Aβ production and attenuating its aggregation, and they caution that a therapeutic intervention simply reducing p 75NTR may exacerbate AD pathology.
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Precursor of Brain-derived Neurotrophic Factor (proBDNF) Forms a Complex with Huntingtin-associated Protein-1 (HAP1) and Sortilin That Modulates proBDNF Trafficking, Degradation, and Processing

TL;DR: It is reported that proBDNF forms a complex with Huntingtin associated protein-1 (HAP1) and sortilin, which plays an important role in proBD NF intracellular trafficking and stabilization, and the complex facilitates furin cleavage to release mature BDNF.
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ProBDNF and its receptors are upregulated in glioma and inhibit the growth of glioma cells in vitro.

TL;DR: The expression levels of proBDNF, p75NTR, and sortilin were significantly increased in high-grade glioma and were positively correlated with the malignancy of the tumor.
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Direct Reprogramming of Mouse Fibroblasts to Neural Stem Cells by Small Molecules.

TL;DR: A novel way to efficiently induce neural stem cells (iNSC) from fibroblasts using only small molecules without altering the genome is established, which may enable NSC to be utilized in various applications within clinical medicine.
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Amyloid beta1–42 (Aβ42) up‐regulates the expression of sortilin via the p75NTR/RhoA signaling pathway

TL;DR: It is shown that sortilin expression is increased in the AD brain in human and mice and that Aβ42 oligomer increasessortilin gene and protein expression through p75NTR and RhoA signaling pathways, suggesting a potential physiological interaction of Aβ 42 and sortilIn in Alzheimer's disease.