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Giovanni Antico, PhD
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• Dr. Charles Clevenger Lab • Post Doctoral Fellow
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Topic:
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"Vav2 and Nek3 in the Prolactin-mediated actions in breast cancer cells: cytoplasmic and nuclear functions" |
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Our laboratory has shown that Vav2 is linked to prolactin (PRL) signaling in breast cancer cells, and that Vav2 is a serine-kinase substrate of Nek3, a member of the NIMA family proteins activated by PRL. Both Nek3 and Vav2 were found associated with PRL receptor upon ligand binding, and were involved in the PRL-induced cytoskeletal re-organization via Rac1. Vav2 contains a putative nuclear localization sequence. The presence of Vav2 and Nek3 in the nucleus is confirmed by IHC and CoIP analyses. Upon PRL stimulation, Vav2 and Nek3 associate with the promoter of CyclinD1 gene and the time profile is similar to that of the transcription factors STAT5 and NFAT1. CyclinD1 gene is known to be regulated by PRL and probably involved in the development and/or progression of mammary cancer. Finally, both Vav2 and Nek3 can immunoprecipitate with STAT5 and NFAT1, and Vav2 can interfere, in reporter assays, with their transcriptional activities.
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Gregory J. Woodhead
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• Dr. Anjen Chenn Lab • Graduate Student
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Topic:
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"N-cadherin regulates tissue architecture and ß-catenin signaling in the cortical progenitor niche" |
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Progenitor cells in developing organisms reside in complex environments that can regulate their proliferation and differentiation. Focal reduction of N-cadherin in the developing brain causes both loss of tissue architecture and cell-autonomous changes in cell fate. Further, in vivo knockdown of N-cadherin leads to reduction in ß-catenin signaling. In areas of tissue disruption, cell differentiation appears to be disrupted in a non cell-autonomous fashion. In contrast, cell autonomous reduction of N-cadherin or ß-catenin signaling in a normal tissue context causes premature exit of cells from the progenitor zone and increased differentiation. These results show that Ncadherin regulates neural progenitor cell fate both by regulating tissue architecture and by controlling ß-catenin signaling and suggest that neural progenitor cells can function to generate a self-supportive local environment to regulate their own proliferation.
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When:
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Monday, March 5, 2007
12:00PM – 1:00PM
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Location:
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Baldwin Auditorium
Robert H. Lurie Medical Research Center
303 East Superior Street, 1st floor |
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