Linked Life Data

20023420

Source:http://linkedlifedata.com/resource/pubmed/id/20023420

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-1-22
pubmed:abstractText
Autophagy is commonly characterized by the redistribution of the microtubule-associated light chain 3 (LC3) protein into cytoplasmic puncta, coinciding with its lipidation, as well as by a decrease in the abundance of autophagic substrates including p62 and ubiquitinylated proteins. Here, we describe a cell line, A549-B480, which, in contrast to its parental A549 line, exhibits massive accumulation of LC3 (or a GFP-LC3 fusion protein) in cytoplasmic puncta. These puncta co-localize with accumulated p62 and ubiquitinylated proteins, yet are not enwrapped by membranes. Indeed, LC3 is not lipidated in A549-B480, even when these cells are cultured in conditions in which A549 cells would develop autophagy. A549-B480 cells have been selected for their resistance against the microtubule-stabilizing agent epothilone B and actually require the continuous presence of epothilone B for their survival. Parental A549 cells treated with epothilone B manifested all signs of bona fide autophagy. In contrast, the autophagic program of A549-B480 was defective, irrespective of the absence or presence of epothilone B, and correlated with the complete absence of Atg7, a protein that is reputed to be essential for autophagy. These results establish novel functional links between microtubules and autophagy, identify a new chemotherapy resistance-associated autophagic defect, and describe the existence of LC3 puncta outside from autophagosomes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
377-83
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Defective autophagy associated with LC3 puncta in epothilone-resistant cancer cells.
pubmed:affiliation
INSERM U848, Institut Gustave Roussy and Université Paris Sud-XI, Villejuif, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't