Aureobasidin A(AbA)金担子素A

Aureobasidin A(AbA)金担子素A

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  • ¥950
  • Clontech
  • clontech
  • 630466
  • 2025年09月28日
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    • 详细信息
    • 询价记录
    • 技术资料
    • 英文名

      Aureobasidin A

    • 库存

      现货

    • 供应商

      上海伟进科技有限公司

    • 规格

      1mg

    Aureobasidin A for Yeast Two-Hybrid Studies

    Aureobasidin A (AbA) is a cyclic depsipeptide antibiotic, isolated from the filamentous fungusAureobasidium pullulans R106, which is toxic to yeast at low concentrations (0.1–0.5 µg/ml). Sensitive species include Saccharomyces cerevisiae, Schizosaccharomyces pombe, Candida glabrata, Aspergillus nidulans, and A. niger.

    AbA inhibits a yeast enzyme, inositol phosphorylceramide (IPC) synthase, which is expressed from the AUR1 gene (1, 2). Expression of a mutant gene, AUR1-C, in transformed yeast confers resistance to the drug. It is this gene that is used in Matchmaker Gold systems as a reporter for protein interactions.

    Perfect Reporter for Yeast Two-Hybrid Studies

    AbA selection virtually eliminates the high numbers of background colonies that often plague low-stringency primary screens that use nutritional markers alone (e.g. HIS3). Because AbA actually kills sensitive yeast cells, rather than merely retarding their growth, AbA-based selection greatly favors the growth and identification of genuinely positive clones. In general practice, a high percentage of clones that emerge from low-stringency primary screens using AbA selection alone, are subsequently verified on high-stringency secondary screens that select for all four Matchmaker Gold reporters (AUR1-C,HIS3, ADE2 and MEL1).

    Features

    • Stringent drug-selectable marker for yeast
    • Aureobasidin A resistance is an ideal reporter for yeast two-hybrid studies
    • Provides exceptional screening results with Matchmaker Gold Yeast One- and Two-Hybrid Systems

    Applications

    • Yeast Two-Hybrid Studies
    • Yeast One-Hybrid Studies

    Properties

    • Molecular Weight 1100 Da
    • Insoluble in water

    References

    1. Takesako, K. et al. (1993) J. Antibiot. (Tokyo) 46(9):1414–20.
    2. Hashida-Okado, T. et al. (1996) Mol. Gen. Genet. 251(2):236–244.

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