Anti-Bcl-2 (phospho T56) 抗体 (ab28820)


  • 製品名Anti-Bcl-2 (phospho T56) antibody
    Bcl-2 一次抗体 製品一覧
  • 製品の詳細
    Rabbit polyclonal to Bcl-2 (phospho T56)
  • 特異性ab28820 recognises Phospho-BCL-2(Thr56)
  • アプリケーション適用あり: IHC-P, ELISA, ICC/IF, WBmore details
  • 種交差性
    交差種: Human
  • 免疫原

    Synthetic peptide corresponding to Human Bcl-2.
    Database link: P10415

  • ポジティブ・コントロール
    • Breast carcinoma




Our Abpromise guarantee covers the use of ab28820 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
IHC-P Use at an assay dependent concentration.
ELISA 1/20000.
ICC/IF 1/100 - 1/500.
WB 1/500 - 1/1000.


  • 機能Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release (PubMed:17418785).
  • 組織特異性Expressed in a variety of tissues.
  • 関連疾患A chromosomal aberration involving BCL2 has been found in chronic lymphatic leukemia. Translocation t(14;18)(q32;q21) with immunoglobulin gene regions. BCL2 mutations found in non-Hodgkin lymphomas carrying the chromosomal translocation could be attributed to the Ig somatic hypermutation mechanism resulting in nucleotide transitions.
  • 配列類似性Belongs to the Bcl-2 family.
  • ドメインBH1 and BH2 domains are required for the interaction with BAX and for anti-apoptotic activity.
    The BH4 motif is required for anti-apoptotic activity and for interaction with RAF1 and EGLN3.
    The loop between motifs BH4 and BH3 is required for the interaction with NLRP1.
  • 翻訳後修飾Phosphorylation/dephosphorylation on Ser-70 regulates anti-apoptotic activity. Growth factor-stimulated phosphorylation on Ser-70 by PKC is required for the anti-apoptosis activity and occurs during the G2/M phase of the cell cycle. In the absence of growth factors, BCL2 appears to be phosphorylated by other protein kinases such as ERKs and stress-activated kinases. Phosphorylated by MAPK8/JNK1 at Thr-69, Ser-70 and Ser-87, wich stimulates starvation-induced autophagy. Dephosphorylated by protein phosphatase 2A (PP2A).
    Proteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity, causes the release of cytochrome c into the cytosol promoting further caspase activity.
    Monoubiquitinated by PARK2, leading to increase its stability. Ubiquitinated by SCF(FBXO10), leading to its degradation by the proteasome.
  • 細胞内局在Mitochondrion outer membrane. Nucleus membrane. Endoplasmic reticulum membrane.
  • Information by UniProt
  • 参照データベース
  • 別名
    • Apoptosis regulator Bcl 2 antibody
    • Apoptosis regulator Bcl-2 antibody
    • Apoptosis regulator Bcl2 antibody
    • AW986256 antibody
    • B cell CLL/lymphoma 2 antibody
    • B cell leukemia/lymphoma 2 antibody
    • Bcl-2 antibody
    • Bcl2 antibody
    • BCL2_HUMAN antibody
    • C430015F12Rik antibody
    • D630044D05Rik antibody
    • D830018M01Rik antibody
    • Leukemia/lymphoma, B-cell, 2 antibody
    • Oncogene B-cell leukemia 2 antibody
    • PPP1R50 antibody
    • Protein phosphatase 1, regulatory subunit 50 antibody
    see all

Anti-Bcl-2 (phospho T56) antibody 画像

  • Immunohistochemical analysis of paraffin-embedded breast carcinoma, using Anti-Phospho-BCL2(Thr56) Antibody (ab28820). Left: Untreated; Right: Treated with synthesized phospho-peptide.

  • Immunofluorescence analysis of A549 cells, using ab28820.
    The Image on the right is treated with the synthesized peptide.

Anti-Bcl-2 (phospho T56) antibody (ab28820) 使用論文

ab28820 has not yet been referenced specifically in any publications.

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