کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1950669 | 1537957 | 2012 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Impaired c-src activation and motility defects in PEA3-null fibroblasts Impaired c-src activation and motility defects in PEA3-null fibroblasts](/preview/png/1950669.png)
Null mutations in the pea3 allele compromise the capacity of mammary tumors to metastasize in MMTV-Neu/ErbB2/HER2 transgenic mice, indicating a motility defect in PEA3-null cells. Cellular and biochemical analyses of established PEA3-null fibroblasts show impaired motility and aberrant localization of adhesion proteins in spreading cells. Our results show that PEA3 −/− cells express normal levels of key adhesion components, but that spreading PEA3-null cells fail to activate c-src and to downregulate phospho-FAK(Y397), suggesting that focal adhesion signaling is impaired. Supporting this, biochemical analysis revealed that adhesion complex-associated proteins such as p130Cas failed to undergo tyrosine phosphorylation and dissociated from the adhesion complex with delayed kinetics. Overall our data show that the motility defects observed in PEA3-null cells are due to altered adhesion signaling.
► We show a reduction in focal adhesions and actin stress fibers in PEA3-null cells.
► Our study show motility defects in these cells on fibronectin-coated substrates.
► We show that these cells have defects in c-src activation and FAK tyrosine phosphorylation.
► Our data show that these cells have impaired adhesion complex activation and disassembly.
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1823, Issue 12, December 2012, Pages 2237–2242