Title |
Stat3 is a positive regulator of gap junctional intercellular communication in cultured, human lung carcinoma cells
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Published in |
BMC Cancer, December 2012
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DOI | 10.1186/1471-2407-12-605 |
Pubmed ID | |
Authors |
Mulu Geletu, Rozanne Arulanandam, Samantha Greer, Aaron Trotman-Grant, Evangelia Tomai, Leda Raptis |
Abstract |
Neoplastic transformation of cultured cells by a number of oncogenes such as src suppresses gap junctional, intercellular communication (GJIC); however, the role of Src and its effector Signal transducer and activator of transcription-3 (Stat3) upon GJIC in non small cell lung cancer (NSCLC) has not been defined. Immunohistochemical analysis revealed high Src activity in NSCLC biopsy samples compared to normal tissues. Here we explored the potential effect of Src and Stat3 upon GJIC, by assessing the levels of tyr418-phosphorylated Src and tyr705-phosphorylated Stat3, respectively, in a panel of NSCLC cell lines. |
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Demographic breakdown
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Members of the public | 1 | 100% |
Mendeley readers
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Unknown | 13 | 87% |
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Professor > Associate Professor | 3 | 20% |
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Other | 1 | 7% |
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Other | 1 | 7% |
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Immunology and Microbiology | 1 | 7% |
Other | 0 | 0% |
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