製品の概要

  • 製品名Anti-IL1 beta antibody
    IL1 beta 一次抗体 製品一覧
  • 製品の詳細
    Rabbit polyclonal to IL1 beta
  • 特異性Ab53175 detects endogenous levels of fragment of activated IL1 beta resulting from cleavage adjacent to Asp116. Ab53175 also detects the uncleaved form in WB.
  • アプリケーション適用あり: WB, IHC-P, ELISAmore details
  • 種交差性
    交差種: Human
  • 免疫原

    Synthetic peptide derived from human IL1 beta.

  • ポジティブ・コントロール
    • Human lung carcinoma tissue.

製品の特性

アプリケーション

Our Abpromise guarantee covers the use of ab53175 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 at an assay dependent concentration.
IHC-P Use at an assay dependent concentration.
ELISA 1/10000.

ターゲット情報

  • 機能Potent proinflammatory cytokine. Initially discovered as the major endogenous pyrogen, induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B-cell activation and antibody production, and fibroblast proliferation and collagen production. Promotes Th17 differentiation of T-cells.
  • 組織特異性Expressed in activated monocytes/macrophages (at protein level).
  • 配列類似性Belongs to the IL-1 family.
  • 翻訳後修飾Activation of the IL1B precursor involves a CASP1-catalyzed proteolytic cleavage. Processing and secretion are temporarily associated.
  • 細胞内局在Cytoplasm, cytosol. Lysosome. Secreted, exosome. Cytoplasmic vesicle, autophagosome. Secreted. The precursor is cytosolic. In response to inflammasome-activating signals, such as ATP for NLRP3 inflammasome or bacterial flagellin for NLRC4 inflammasome, cleaved and secreted. IL1B lacks any known signal sequence and the pathway(s) of its secretion is(are) not yet fully understood (PubMed:24201029). On the basis of experimental results, several unconventional secretion mechanisms have been proposed. 1. Secretion via secretory lysosomes: a fraction of CASP1 and IL1B precursor may be incorporated, by a yet undefined mechanism, into secretory lysosomes that undergo Ca(2+)-dependent exocytosis with release of mature IL1B (PubMed:15192144). 2. Secretory autophagy: IL1B-containing autophagosomes may fuse with endosomes or multivesicular bodies (MVBs) and then merge with the plasma membrane releasing soluble IL1B or IL1B-containing exosomes (PubMed:24201029). However, autophagy impacts IL1B production at several levels and its role in secretion is still controversial. 3. Secretion via exosomes: ATP-activation of P2RX7 leads to the formation of MVBs containing exosomes with entrapped IL1B, CASP1 and other inflammasome components. These MVBs undergo exocytosis with the release of exosomes. The release of soluble IL1B occurs after the lysis of exosome membranes (By similarity). 4. Secretion by microvesicle shedding: activation of the ATP receptor P2RX7 may induce an immediate shedding of membrane-derived microvesicles containing IL1B and possibly inflammasome components. The cytokine is then released in the extracellular compartment after microvesicle lysis (PubMed:11728343). 5. Release by translocation through permeabilized plasma membrane. This may occur in cells undergoing pyroptosis due to sustained activation of the inflammasome (By similarity). These mechanisms may not be not mutually exclusive.
  • Information by UniProt
  • 参照データベース
  • 別名
    • Catabolin antibody
    • H1 antibody
    • IL 1 antibody
    • IL 1 beta antibody
    • IL-1 beta antibody
    • IL1 BETA antibody
    • IL1B antibody
    • IL1B_HUMAN antibody
    • IL1F2 antibody
    • Interleukin 1 beta antibody
    • Interleukin-1 beta antibody
    • OAF antibody
    • OTTHUMP00000162031 antibody
    • Preinterleukin 1 beta antibody
    • Pro interleukin 1 beta antibody
    see all

Anti-IL1 beta antibody 画像

  • ab53175 at 1/50 dilution staining IL1 beta in human lung carcinoma by Immunohistochemsitry, Paraffin embedded tissue, in the absence or presence of the immunising peptide.

Anti-IL1 beta antibody (ab53175) 使用論文

ab53175 has not yet been referenced specifically in any publications.

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