liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Proteasome inhibition enhances lipofuscin formation
Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
2002 (English)In: Annals of the New York Academy of Sciences, ISSN 0077-8923, E-ISSN 1749-6632, Vol. 973, 309-312 p.Article in journal (Refereed) Published
Abstract [en]

Lipofuscin, a hallmark of aged nondividing cells, is an undegradable autofluorescent intralysosomal substance composed essentially of oxidized, cross-linked proteins. To test whether impaired activity of proteasomes-which, along with lysosomes, belong to major cellular proteolytic systems-may contribute to lipofuscinogenesis, we exposed growth-arrested human fibroblasts to subapoptotic doses (2 and 5 nM) of a highly specific proteasome inhibitor, MG-262. This resulted in accelerated lipofuscin accumulation (especially when MG-262 exposure was combined with mild hyperoxia cultivation at 40% ambient oxygen versus 8% for controls), and enhanced immunostaining for ubiquitin, reflecting accumulation of modified cytosolic proteins subjected for degradation, and cathepsin L, reflecting enlargement of the lysosomal compartment. These data suggest that insufficient proteasomal function may contribute to lipofuscinogenesis by a compensatory increase in the amount of proteins that are difrected for lysosomal degradation. The findings may be helpful for the understanding of cellular aging as well as diseases associated with intralysosomal accumulation of undegradable material.

Place, publisher, year, edition, pages
2002. Vol. 973, 309-312 p.
Keyword [en]
aging, fibroblasts, lipofuscin, lysosomes, proteasomes, proteolysis
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-27935Local ID: 12696OAI: oai:DiVA.org:liu-27935DiVA: diva2:248487
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2017-12-13

Open Access in DiVA

No full text

Authority records BETA

Terman, Alexei

Search in DiVA

By author/editor
Terman, Alexei
By organisation
Faculty of Health SciencesPathology
In the same journal
Annals of the New York Academy of Sciences
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

urn-nbn

Altmetric score

urn-nbn
Total: 44 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf