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Issue 7, 2014
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Role of cytoskeletal proteins in cerebral cavernous malformation signaling pathways: a proteomic analysis

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Abstract

Three genetic mutations were found to cause cerebral cavernous malformation (CCM), a vascular anomaly predisposing affected individuals to hemorrhagic stroke. These CCM proteins function together as a protein complex in the cell. Loss of expression of each CCM gene results in loss of in vitro endothelial tube formation. Label-free differential protein expression analysis using multidimensional liquid chromatography/tandem mass spectrometry (2D-LC-MS/MS) was applied to explore the proteomic profile for loss of each CCM gene expression in mouse endothelial stem cells (MEES) compared to mock shRNA and no shRNA control cell-lines. Differentially expressed proteins were identified (p < 0.05). 120 proteins were differentially expressed among the cell-lines. Principal component analysis and cluster analysis show the effects of individual knockdown. In all knockdown cell-lines, altered expression of cytoskeletal proteins is the most common. While all CCM mutations result in similar pathology, different CCM mutations have their own distinct pathogenesis in cell signaling.

Graphical abstract: Role of cytoskeletal proteins in cerebral cavernous malformation signaling pathways: a proteomic analysis

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Publication details

The article was received on 24 May 2013, accepted on 16 Apr 2014 and first published on 17 Apr 2014


Article type: Paper
DOI: 10.1039/C3MB70199A
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Citation: Mol. BioSyst., 2014,10, 1881-1889
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    Role of cytoskeletal proteins in cerebral cavernous malformation signaling pathways: a proteomic analysis

    S. S. Baxter, C. F. Dibble, W. C. Byrd, J. Carlson, C. R. Mack, I. Saldarriaga and S. Bencharit, Mol. BioSyst., 2014, 10, 1881
    DOI: 10.1039/C3MB70199A

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