AIRE Polyclonal Antibody

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  • 抗体类型:多克隆
  • 抗体来源:
  • 抗体应用:WB, IF
  • 特异性:Human, Mouse

产品详情

  • 产品名称
    AIRE Polyclonal Antibody
  • 抗体类型
    多克隆
  • 抗体来源
  • 抗体亚型
    兔IgG
  • 抗体描述
    Polyclonal antibody to AIRE
  • 抗体应用
    WB, IF
  • 应用推荐
    WB 1:500 - 1:2000
    IF 1:50 - 1:200
  • 特异性
    Human, Mouse
  • 蛋白别名
    AIRE, AIRE1, APECED, APS1, APSI, PGA1, autoimmune regulator
  • 制备方法
    Antigen: A synthetic peptide corresponding to a sequence within amino acids 30-130 of human AIRE (NP_000374.1).
  • 组分
    PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
  • 储存方法
    Store at -20℃. Avoid freeze / thaw cycles.
  • 背景介绍
    Transcription factor playing an essential role to promote self-tolerance in the thymus by regulating the expression of a wide array of self-antigens that have the commonality of being tissue-restricted in their expression pattern in the periphery, called tissue restricted antigens (TRA). Binds to G-doublets in an A/T-rich environment; the preferred motif is a tandem repeat of 5'-ATTGGTTA-3' combined with a 5'-TTATTA-3' box. Binds to nucleosomes (By similarity). Binds to chromatin and interacts selectively with histone H3 that is not methylated at 'Lys-4', not phosphorylated at 'Thr-3' and not methylated at 'Arg-2'. Functions as a sensor of histone H3 modifications that are important for the epigenetic regulation of gene expression. Mainly expressed by medullary thymic epithelial cells (mTECs), induces the expression of thousands of tissue-restricted proteins, which are presented on major histocompatibility complex class I (MHC-I) and MHC-II molecules to developing T-cells percolating through the thymic medulla. Also induces self-tolerance through other mechanisms such as the regulation of the mTEC differentiation program. Controls the medullary accumulation of thymic dendritic cells and the development of regulatory T-cell through the regulation of XCL1 expression. Regulates the production of CCR4 and CCR7 ligands in medullary thymic epithelial cells and alters the coordinated maturation and migration of thymocytes. In thimic B-cells, allows the presentation of licensing-dependent endogenous self-anitgen for negative selection. In secondary lymphoid organs, induces functional inactivation of CD4(+) T-cells. Expressed by a distinct bone marrow-derived population, induces self-tolerance through a mechanism that does not require regulatory T-cells and is resitant to innate inflammatory stimuli (By similarity).
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