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Title:New insights into autophagic cell death in the gypsy moth Lymantria dispar: a proteomic approach.
Authors:Malagoli, Davide (Author)
Boraldi, Federica (Author)
Annovi, Giulia (Author)
Quaglino, Daniela (Author)
Ottaviani, Enzo (Author)
Files:This document has no files. This document may have a phisical copy in the library of the organization, check the status via COBISS. Link is opened in a new window
Language:English
Work type:Not categorized (r6)
Tipology:1.01 - Original Scientific Article
Organization:UNG - University of Nova Gorica
Abstract:Autophagy is an evolutionary ancient process based on the activity of genes conserved from yeast to metazoan taxa. Whereas its role as a mechanism to provide energy during cell starvation is commonly accepted, debate continues about the occurrence of autophagy as a means specifically activated to achieve cell death. The IPLB-LdFB insect cell line, derived from the larval fat body of the lepidoptera Lymantria dispar, represents a suitable model to address this question, as both autophagic and apoptotic cell death can be induced by various stimuli. Using morphological and functional approaches, we have observed that the culture medium conditioned by IPLB-LdFB cells committed to death by the ATPase inhibitor oligomycin A stimulates autophagic cell death in untreated IPLB-LdFB cells. Moreover, proteomic analysis of the conditioned media suggests that, in IPLB-LdFB cells, oligomycin A promotes a shift towards lipid metabolism, increases oxidative stress and specifically directs the cells towards autophagic activity.
Keywords:Autophagic cell death, Fat body, IDGF, IPLB-LdFB, Proteomics
Year of publishing:2009
Number of pages:107-118
Numbering:336
COBISS_ID:5439227 Link is opened in a new window
URN:URN:SI:UNG:REP:IGMCPL3D
DOI:10.1007/s00441-008-0748-8  Link is opened in a new window
License:CC BY-NC-ND 4.0
This work is available under this license: Creative Commons Attribution Non-Commercial No Derivatives 4.0 International
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Record is a part of a journal

Title:Cell and Tissue Research
Year of publishing:2009

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