| First Author | Chaar ZY | Year | 2012 |
| Journal | Biochim Biophys Acta | Volume | 1823 |
| Issue | 12 | Pages | 2237-42 |
| PubMed ID | 22982417 | Mgi Jnum | J:192902 |
| Mgi Id | MGI:5466794 | Doi | 10.1016/j.bbamcr.2012.09.002 |
| Citation | Chaar ZY, et al. (2012) Impaired c-src activation and motility defects in PEA3-null fibroblasts. Biochim Biophys Acta 1823(12):2237-42 |
| abstractText | 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. |
