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TBK1 Kinase Addiction in Lung Cancer Cells Is Mediated via Autophagy of Tax1bp1/Ndp52 and Non-Canonical NF-κB Signalling

Overview of attention for article published in PLOS ONE, November 2012
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Title
TBK1 Kinase Addiction in Lung Cancer Cells Is Mediated via Autophagy of Tax1bp1/Ndp52 and Non-Canonical NF-κB Signalling
Published in
PLOS ONE, November 2012
DOI 10.1371/journal.pone.0050672
Pubmed ID
Authors

Alice C. Newman, Caroline L. Scholefield, Alain J. Kemp, Michelle Newman, Edward G. McIver, Ahmad Kamal, Simon Wilkinson

Abstract

K-Ras dependent non-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellular metabolism in a lysosomal-sensitive manner. Here we demonstrate that the xenophagy-associated kinase TBK1 drives basal autophagy, consistent with its known requirement in K-Ras-dependent NSCLC proliferation. Furthermore, basal autophagy in this context is characterised by sequestration of the xenophagy cargo receptor Ndp52 and its paralogue Tax1bp1, which we demonstrate here to be a bona fide cargo receptor. Autophagy of these cargo receptors promotes non-canonical NF-κB signalling. We propose that this TBK1-dependent mechanism for NF-κB signalling contributes to autophagy addiction in K-Ras driven NSCLC.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 86 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 1%
Unknown 85 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 22 26%
Researcher 15 17%
Student > Master 10 12%
Professor > Associate Professor 6 7%
Student > Bachelor 4 5%
Other 14 16%
Unknown 15 17%
Readers by discipline Count As %
Agricultural and Biological Sciences 27 31%
Biochemistry, Genetics and Molecular Biology 25 29%
Immunology and Microbiology 6 7%
Neuroscience 4 5%
Medicine and Dentistry 3 3%
Other 3 3%
Unknown 18 21%