製品の概要

  • 製品名Anti-AtAGB1 antibody [AGB1-47]
  • 製品の詳細
    Mouse monoclonal [AGB1-47] to AtAGB1
  • 特異性This antibody reacts with AtAGB1. It does not cross react with AtAGG1.
  • アプリケーション適用あり: WB, Indirect ELISAmore details
  • 種交差性
    交差種: Arabidopsis thaliana
  • 免疫原

    Synthetic peptide:

    DSNLKIWAFGGHRRVI

    conjugated to KLH, corresponding to amino acids 362-377 of Arabidopsis thaliana AtAGB1

製品の特性

アプリケーション

Our Abpromise guarantee covers the use of ab55905 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

アプリケーション Abreviews 特記事項
WB Use a concentration of 0.5 - 1 µg/ml. Detects a band of approximately 40 kDa.
Indirect ELISA Use at an assay dependent dilution.

ターゲット情報

  • 関連性Signaling through G-proteins is highly conserved in eukaryotes. G-proteins are responsible for transferring extracellular signals from cell-surface receptors. Upon ligand binding to G-protein coupled receptor (GPCR) there is a GDP/GTP exchange on the a-subunit of G proteins (Ga), causing a dissociation of Ga- from Gbg dimer. The Arabidopsis genome contains genes encoding one G-protein a-subunit (GPA1), one b-subunit (AGB1), and two g-subunits (AGG1 and AGG2). Studies on the null alleles of GPA1 and AGB1 showed that plants use heterotrimeric G-protein signaling in several growth and developmental processes. Abscisic acid (ABA) regulates many physiological processes like seed germination, early seeding development, stomatal guard cell functions and acclimation to adverse environmental conditions. Knocking out GPA1 and/or AGB1 in Arabidopsis plants negatively regulates abscisic acid signaling in seed germination and in early seedling development. The lack of AGB1 causes a greater ABA hypersensitivity than the lack of GPA1, suggesting that AGB1 is the predominant regulator of ABA signaling.
  • 参照データベース

    Anti-AtAGB1 antibody [AGB1-47] (ab55905) 使用論文

    ab55905 has not yet been referenced specifically in any publications.

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