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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2001-8-27
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pubmed:abstractText |
Recently, several members of the claudin family have been identified as integral constituents of tight junctions. Using expression profiling, we previously found claudin-4 to be overexpressed in pancreatic cancer. Because claudin-4 has been described as a receptor for the cytotoxic Clostridium perfringens enterotoxin (CPE), we investigated the effect of CPE on pancreatic cancer cells.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0016-5085
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
121
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
678-84
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11522752-Adenocarcinoma,
pubmed-meshheading:11522752-Animals,
pubmed-meshheading:11522752-Carcinoma, Pancreatic Ductal,
pubmed-meshheading:11522752-Dose-Response Relationship, Drug,
pubmed-meshheading:11522752-Enterotoxins,
pubmed-meshheading:11522752-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:11522752-Humans,
pubmed-meshheading:11522752-Membrane Proteins,
pubmed-meshheading:11522752-Mice,
pubmed-meshheading:11522752-Mice, Nude,
pubmed-meshheading:11522752-Neoplasm Transplantation,
pubmed-meshheading:11522752-Pancreatic Neoplasms,
pubmed-meshheading:11522752-RNA, Messenger,
pubmed-meshheading:11522752-Tight Junctions,
pubmed-meshheading:11522752-Transforming Growth Factor beta,
pubmed-meshheading:11522752-Transplantation, Heterologous,
pubmed-meshheading:11522752-Tumor Cells, Cultured
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pubmed:year |
2001
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pubmed:articleTitle |
Claudin-4: a new target for pancreatic cancer treatment using Clostridium perfringens enterotoxin.
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pubmed:affiliation |
Department of Internal Medicine I, University Medical Center, University of Ulm, Ulm, Germany.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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