作者: Susann-Brady Kalnay
DOI:
关键词: Tyrosine phosphorylation 、 Cell adhesion 、 Cancer research 、 Neural cell adhesion molecule 、 Cell growth 、 Cell adhesion molecule 、 Cell surface receptor 、 Protein tyrosine phosphatase 、 Biology 、 Cell biology 、 Cancer cell
摘要: Abstract : The purpose of this research is to understand how cell adhesion-induced signals are transduced negatively regulate growth and process altered in prostate cancer. Extracellular events that transmitted by changes tyrosine phosphorylation, which controlled protein kinases (PTKs) phosphatases (PTPs). Cancer causing genes encode PTKs cause uncontrolled suggesting PTPs play a role negative regulation or function as tumor suppressors. Both adhesion molecules phosphorylation contact inhibition growth, i.e. when normal cells stop growing because they adjacent cells. Prostate cancer have defects both growth. receptor PTP, PTP mu, directly interacts with E-cadherin, the major cell-cell molecule Loss components cadherin pathway has previously been observed We recently demonstrated PTPmu no longer expressed Re-expression restores regulates A detailed analysis alters adhesion, signal transduction described provides insights into well malignant transformation