EGFR-Dependent Regulation of Matrix-Independent Epithelial Cell Survival
作者： Ulrich Rodeck , THOMAS JEFFERSON UNIV PHILADELPHIA PA
DOI: 10.21236/ADA426140
关键词:
摘要: Abstract : Signaling through the epidermal growth factor (EGFR) has been implicated in both effective wound healing and epithelial neoplasia. We have identified a novel function of EGFR support cell survival, particularly conditions anchorage-independence. Furthermore, we MEK/MAPK signaling this process. Objective/hypothesis: Define molecular mechanisms pathways by which activation supports survival. Two specific aims focus on (1) posttranslational modification relevant Bcl-2 family members MAPK-dependent and, (2) STAT3 deregulated as observed cancer. Progress: During funding period from March, 2004 to 2005 completed study BIM, pro-apoptotic member ERK/MAPK. This work is SA1 original application submitted currently being revised be published Oncogene. In addition, further characterized MAPKinases JNK p38 it relates to- anchorage-independent state.
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