Par-4 Is an Essential Downstream Target of DAP-like Kinase (Dlk) in Dlk/Par-4–mediated Apoptosis
作者： Meike Boosen , Susanne Vetterkind , Jan Kubicek , Karl-Heinz Scheidtmann , Susanne Illenberger
关键词: Myosin light-chain kinase 、 Apoptosis 、 Molecular biology 、 Actin 、 Biology 、 Phosphorylation 、 Kinase 、 Calcium-Calmodulin-Dependent Protein Kinases 、 Kinase activity 、 Protein kinase A
摘要: Prostate apoptosis response-4 (Par-4) was initially identified as a gene product up-regulated in prostate cancer cells undergoing apoptosis. In rat fibroblasts, coexpression of Par-4 and its interaction partner DAP-like kinase (Dlk, which is also known zipper-interacting protein [ZIPK]) induces relocation the from nucleus to actin filament system, followed by extensive myosin light chain (MLC) phosphorylation induction Our analyses show that synergistic proapoptotic effect Dlk/Par-4 complexes abrogated when either or Dlk activity impaired. vitro assays employing mutants carrying alanine substitutions for residues S154, T155, S220, S249, respectively, T155 major site Dlk. Coexpression experiments REF52.2 revealed at essential vivo. presence T155A mutant partially recruited filaments but resided mainly nucleus. Consequently, not induced T155A-expressing cells. vivo demonstrated with phospho-specific antibody. results demonstrate Dlk-mediated crucial event Dlk/Par-4-induced
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