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1 was homologous to sequences of other fungal aspartyl proteinases.
2 ida albicans that were deficient in secreted aspartyl proteinase 1 (Sap1), Sap2, or Sap3 were investi
6 ogenic cells resists inhibitors of serine or aspartyl proteinases as well as tissue inhibitor of matr
7 llmark of tumor invasion and metastasis, and aspartyl proteinase cathepsin D is implicated as a major
9 us mutants deficient in one or more secreted aspartyl proteinases encoded by SAP genes or in transcri
10 enetic analysis of the ALS and SAP (secreted aspartyl proteinase) families show that the ALS family i
11 structure for the possible evolution of the aspartyl proteinase family, with particular reference to
12 f intron positions and intron phases between aspartyl proteinases from nematodes and apicomplexans.
13 lytic gene expression, we compared secretory aspartyl proteinase gene (SAP) and phospholipase B gene
15 c gene PEP1 (SAP1), which encodes a secreted aspartyl proteinase, in the expression of the unique opa
16 ed the role of Candida parapsilosis-secreted aspartyl proteinase isoenzyme 1 (SAPP1) in virulence.
19 ony appearances, mating competency, secreted aspartyl proteinase (Sap) activities, and virulence.
20 vivo expression of Candida albicans secreted aspartyl proteinase (SAP1-SAP8) and phospholipase B (PLB
21 phal-specific virulence factors, such as the aspartyl proteinases Sap4 and Sap5 and the proposed inva
24 ene of C. albicans encodes a unique secreted aspartyl proteinase that contributes to corneal pathogen
25 ntified substrates, including eight secreted aspartyl proteinases, the exoglucanase Xog1p, the immuno
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