2 research outputs found

    Overlapping peptide arrays were made and acetylated in microtiter plates using human EGF receptor residues 622–1186 (Swissprot database locus P0053 with leader sequence removed)

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    <p><b>Copyright information:</b></p><p>Taken from "Fully automated synthesis of (phospho)peptide arrays in microtiter plate wells provides efficient access to protein tyrosine kinase characterization"</p><p>BMC Immunology 2005;6():1-1.</p><p>Published online 12 Jan 2005</p><p>PMCID:PMC546003.</p><p>Copyright © 2005 Saxinger et al; licensee BioMed Central Ltd.</p> Each array contained exclusively tyrosine or phosphotyrosine peptides and was composed of 92 peptides each of which was 21 amino acids long and offset from its neighbor by 6 amino acids. Array peptide wells were reacted in multiplexed ELISA format with antibody 9H2 as described in Methods. Data are plotted without any corrections. Peptide sequences and raw data are listed [see ]

    BRCA1 deficiency in ovarian cancer is associated with alteration in expression of several key regulators of cell motility – A proteomics study

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    <p>Functional loss of expression of breast cancer susceptibility gene 1(<i>BRCA1</i>) has been implicated in genomic instability and cancer progression. There is emerging evidence that <i>BRCA1</i> gene product (BRCA1) also plays a role in cancer cell migration. We performed a quantitative proteomics study of EOC patient tumor tissues and identified changes in expression of several key regulators of actin cytoskeleton/cell adhesion and cell migration (CAPN1, 14-3-3, CAPG, PFN1, SPTBN1, CFN1) associated with loss of BRCA1 function. Gene expression analyses demonstrate that several of these proteomic hits are differentially expressed between early and advanced stage EOC thus suggesting clinical relevance of these proteins to disease progression. By immunohistochemistry of ovarian tumors with BRCA1<sup>+/+</sup> and BRCA1<sup>null</sup> status, we further verified our proteomic-based finding of elevated PFN1 expression associated with BRCA1 deficiency. Finally, we established a causal link between PFN1 and BRCA1-induced changes in cell migration thus uncovering a novel mechanistic basis for BRCA1-dependent regulation of ovarian cancer cell migration. Overall, findings of this study open up multiple avenues by which BRCA1 can potentially regulate migration and metastatic phenotype of EOC cells.</p
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