Document Detail


Removal of the glycosylation of prion protein provokes apoptosis in SF126.
MedLine Citation:
PMID:  17927898     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although the function of cellular prion protein (PrPc) and the pathogenesis of prion diseases have been widely described, the mechanisms are not fully clarified. In this study, increases of the portion of non-glycosylated prion protein deposited in the hamster brains infected with scrapie strain 263K were described. To elucidate the pathological role of glycosylation profile of PrP, wild type human PrP (HuPrP) and two genetic engineering generated non-glycosylated PrP mutants (N181Q/N197Q and T183A/T199A) were transiently expressed in human astrocytoma cell line SF126. The results revealed that expressions of non-glycosylated PrP induced significantly more apoptosis cells than that of wild type PrP. It illustrated that Bcl-2 proteins might be involved in the apoptosis pathway of non-glycosylated PrPs. Our data highlights that removal of glycosylation of prion protein provokes cells apoptosis.
Authors:
Lan Chen; Yang Yang; Jun Han; Bao-Yun Zhang; Lin Zhao; Kai Nie; Xiao-Fan Wang; Feng Li; Chen Gao; Xiao-Ping Dong; Cai-Min Xu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of biochemistry and molecular biology     Volume:  40     ISSN:  1225-8687     ISO Abbreviation:  J. Biochem. Mol. Biol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-10-11     Completed Date:  2008-01-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9702084     Medline TA:  J Biochem Mol Biol     Country:  Korea (South)    
Other Details:
Languages:  eng     Pagination:  662-9     Citation Subset:  IM    
Affiliation:
National Laboratory of Medical Molecular Biology, Institute of Basic Medical Science, Chinese Academy of Medical Sciences and Peking Union Medical College, Dong Dan San Tiao 5, Beijing 100005, Peopleos Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / genetics,  physiology*
Blotting, Western
Brain / metabolism*,  pathology
Cell Line, Tumor
Cricetinae
Flow Cytometry
Fluorescent Antibody Technique
Glycosylation
Humans
Membrane Potential, Mitochondrial
Mutation
Nucleotides / metabolism
Plasmids / genetics
PrPSc Proteins / metabolism
Prions / genetics,  metabolism*
Proto-Oncogene Proteins c-bcl-2 / metabolism
Transfection
bcl-2-Associated X Protein / metabolism
Chemical
Reg. No./Substance:
0/Nucleotides; 0/PrPSc Proteins; 0/Prions; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein

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