Proteasome activation as a novel antiaging strategy

δείτε την πρωτότυπη σελίδα τεκμηρίου
στον ιστότοπο του αποθετηρίου του φορέα για περισσότερες πληροφορίες και για να δείτε όλα τα ψηφιακά αρχεία του τεκμηρίου*



Proteasome activation as a novel antiaging strategy

Χονδρογιάννη, Νίκη
Γκόνος, Ευστάθιος

Άρθρο σε επιστημονικό περιοδικό

2008-10


Hoboken
Homeostasis is a key feature of cellular lifespan. Maintenance of cellular homeostasis influences the rate of aging and is determined by several factors, including efficient proteolysis of damaged proteins. Protein degradation is predominately catalyzed by the proteasome. Specifically, the proteasome is responsible for cell clearance of abnormal, denatured or in general damaged proteins as well as for the regulated degradation of short-lived proteins. As proteasome has an impaired function during aging, emphasis has been given recently in identifying ways of its activation. A number of studies have shown that the proteasome can be activated by genetic manipulations as well as by factors that affect its conformation and stability. Importantly the developed proteasome activated cell lines exhibit an extended lifespan. This review article discusses in details the various factors that are involved in proteasome biosynthesis and assembly and how they contribute to its activation. Finally as few natural compounds have been identified having proteasome activation properties, we discuss the advantages of this novel antiaging strategy.

Βιολογία (Γενικά) (EL)
Biology (General) (EN)

senescence
homeostasis
proteasome
longevity
aging
protein degradation

Αγγλική γλώσσα

John Wiley & Sons Incorporated


Iubmb Life (formerly Biochemistry and Molecular Biology International) (no Longer Published by Taylor & Francis)

https://rightsstatements.org/page/InC/1.0/?language=en
© 2008 IUBMB.
© 2008 IUBMB. (EN)




*Η εύρυθμη και αδιάλειπτη λειτουργία των διαδικτυακών διευθύνσεων των συλλογών (ψηφιακό αρχείο, καρτέλα τεκμηρίου στο αποθετήριο) είναι αποκλειστική ευθύνη των αντίστοιχων Φορέων περιεχομένου.