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- W1504038105 abstract "Objective: A spontaneously developed obese rat (WNIN/Ob) was established from the existing WNIN rats by selective breeding. The WNIN/Ob rats show accelerated aging and develop age related diseases including neurodegeneration. The main aim is to investigate the role of ubiquitin proteasome system (UPS) in obesity-associated neurodegeneration in WNIN/Ob rat model. Methods: Various components of UPS like ubiquitin, UCHs (ubiquitin C-terminal hydrolases), proteasomal sub-units and endoplasmic reticulum (ER) stress markers were analysed by qRT-PCR and immunoblotting. Chymotrypsin-like activity of proteasome was assayed by fluorometric method. Apoptotis and morphology of neurons in the cerebral cortex was assessed by immunohistochemistry and transmission electron microscopy, respectively. Results: The results indicated dysregulated UPS, increased ER stress and up-regulation of apoptotic regulators in obese rats. Neurons in the cerebral cortex of obese rats showed swollen mitochondria, disrupted ER and degenerating axons, nucleus and finally neurons. It appears UCHL-1 mediated apoptosis through stabilizing p53 as a key factor of neurodegeneration. Conclusion: Alterations in the UPS may be causally related to neurodegeneration in WNIN-obese rat. Further this rat model could be a suitable animal model for investigating the role of UPS in age related neurodegenerative diseases." @default.
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- W1504038105 date "2014-04-01" @default.
- W1504038105 modified "2023-09-27" @default.
- W1504038105 title "Dysregulated ubiquitin proteasome system leads to neurodegeneration in a spontaneous obese rat model (559.1)" @default.
- W1504038105 doi "https://doi.org/10.1096/fasebj.28.1_supplement.559.1" @default.
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