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Bacterial genotoxin...
Bacterial genotoxin triggers FEN1-dependent RhoA activation, cytoskeleton remodeling and cell survival
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Guerra, Lina (author)
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- Guidi, Riccardo (author)
- Karolinska Institutet
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Slot, Ilse (author)
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- Callegari, Simone (author)
- Karolinska Institutet
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Sompallae, Ramakrishna (author)
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Pickett, Carol L. (author)
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- Åström, Stefan (author)
- Stockholms universitet,Wenner-Grens institut
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Eisele, Frederik (author)
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Wolf, Dieter (author)
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- Sjögren, Camilla (author)
- Karolinska Institutet
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- Masucci, Maria G. (author)
- Karolinska Institutet
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- Frisan, Teresa, 1967- (author)
- Karolinska Institutet
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(creator_code:org_t)
- The Company of Biologists, 2011
- 2011
- English.
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In: Journal of Cell Science. - : The Company of Biologists. - 0021-9533 .- 1477-9137. ; 124:16, s. 2735-2742
- Related links:
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http://jcs.biologist...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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https://urn.kb.se/re...
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http://kipublication...
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Abstract
Subject headings
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- The DNA damage response triggered by bacterial cytolethal distending toxins (CDTs) is associated with activation of the actin-regulating protein RhoA and phosphorylation of the downstream-regulated mitogen-activated protein kinase (MAPK) p38, which promotes the survival of intoxicated (i.e. cells exposed to a bacterial toxin) cells. To identify the effectors of this CDT-induced survival response, we screened a library of 4492 Saccharomyces cerevisiae mutants that carry deletions in nonessential genes for reduced growth following inducible expression of CdtB. We identified 78 genes whose deletion confers hypersensitivity to toxin. Bioinformatics analysis revealed that DNA repair and endocytosis were the two most overrepresented signaling pathways. Among the human orthologs present in our data set, FEN1 and TSG101 regulate DNA repair and endocytosis, respectively, and also share common interacting partners with RhoA. We further demonstrate that FEN1, but not TSG101, regulates cell survival, MAPK p38 phosphorylation, RhoA activation and actin cytoskeleton reorganization in response to DNA damage. Our data reveal a previously unrecognized crosstalk between DNA damage and cytoskeleton dynamics in the regulation of cell survival, and might provide new insights on the role of chronic bacteria infection in carcinogenesis.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
- NATURVETENSKAP -- Biologi -- Cellbiologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Cell Biology (hsv//eng)
- NATURVETENSKAP -- Biologi -- Mikrobiologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Microbiology (hsv//eng)
- NATURVETENSKAP -- Biologi -- Genetik (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Genetics (hsv//eng)
Keyword
- Cytolethal distending toxin
- DNA damage
- FEN1
- Cell survival
- TSG101
- RhoA
- Actin cytoskeleton
Publication and Content Type
- ref (subject category)
- art (subject category)
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- By the author/editor
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Guerra, Lina
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Guidi, Riccardo
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Slot, Ilse
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Callegari, Simon ...
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Sompallae, Ramak ...
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Pickett, Carol L ...
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show more...
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Åström, Stefan
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Eisele, Frederik
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Wolf, Dieter
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Sjögren, Camilla
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Masucci, Maria G ...
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Frisan, Teresa, ...
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show less...
- About the subject
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- MEDICAL AND HEALTH SCIENCES
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MEDICAL AND HEAL ...
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and Basic Medicine
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and Cell and Molecul ...
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- NATURAL SCIENCES
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NATURAL SCIENCES
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and Biological Scien ...
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and Cell Biology
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- NATURAL SCIENCES
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NATURAL SCIENCES
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and Biological Scien ...
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and Microbiology
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- NATURAL SCIENCES
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NATURAL SCIENCES
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and Biological Scien ...
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and Genetics
- Articles in the publication
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Journal of Cell ...
- By the university
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Stockholm University
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Umeå University
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Karolinska Institutet