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Articles by X Mao
Total Records ( 2 ) for X Mao
  X Mao , X Nie , F Cao and J. Chen
 

Here we reported that, in Saccharomyces cerevisiae, deleting Swi1 (ScSwi1), a core component in Swi/Snf complex, caused defects of invasive growth, pseudohyphal growth, FLO11 expression, and proper cell separation. Re-introduction of SWI1 into the swi1 mutants could suppress all defects observed. We also showed that overproducing Swi1 could suppress the defect of flo8 cells in pseudohyphal growth in diploids, but not invasive growth in haploids. Overexpression of SWI1 could not bypass the requirement of Ste12 or Tec1 in invasive growth or pseudohyphal growth. We concluded that the Swi/Snf complex was required for FLO11 expression and proper cell separation, and both the FLO8 and STE12 genes should be present for the complex to function for the invasive growth but only the STE12 gene was required for the pseudohyphal growth. Ectopic expression of Candida albicans SWI1 (CaSWI1) could partially complement the defects examined of haploid Scswi1 mutants, but failed to complement the defects examined of diploid Scswi1/Scswi1 mutants. Overexpressing CaSwi1 mitigated invasive and pseudohyphal growth defects resulting from deletions in the MAP kinase and cAMP pathways. The integrity of S. cerevisiae Swi/Snf complex is required for invasive and filamentous growth promoted by overexpressing CaSwi1.

  Q ZhuGe , M Zhong , W Zheng , G. Y Yang , X Mao , L Xie , G Chen , Y Chen , M. T Lawton , W. L Young , D. A Greenberg and K. Jin
 

A role for the Notch signalling pathway in the formation of arteriovenous malformations during development has been suggested. However, whether Notch signalling is involved in brain arteriovenous malformations in humans remains unclear. Here, we performed immunohistochemistry on surgically resected brain arteriovenous malformations and found that, compared with control brain vascular tissue, Notch-1 signalling was activated in smooth muscle and endothelial cells of the lesional tissue. Western blotting showed an activated form of Notch-1 in brain arteriovenous malformations, irrespective of clinical presentation and with or without preoperative embolization, but not in normal cerebral vessels from controls. In addition, the Notch-1 ligands Jagged-1 and Delta-like-4 and the downstream Notch-1 target Hes-1 were increased in abundance and activated in human brain arteriovenous malformations. Finally, increased angiogenesis was found in adult rats treated with a Notch-1 activator. Our findings suggest that activation of Notch-1 signalling is a phenotypic feature of brain arteriovenous malformations, and that activation of Notch-1 in normal vasculature induces a pro-angiogenic state, which may contribute to the development of vascular malformations.

 
 
 
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