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RBPJK Rabbit pAb, AP conjugate

d(bs-2966R-AP)-100ul
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  • ¥2980
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  • bs-2966R-AP
  • 2025年09月30日
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      100ul

    产品编号bs-2966R-AP
    英文名称RBPJK Rabbit pAb, AP conjugated
    中文名称AP标记的Notch转录调控蛋白RBPJK抗体
    英文别名AI843960; CBF 1; CBF-1; CBF1; IGKJRB1; J kappa recombination signal binding protein; J kappa-recombination signal binding protein; J kappa-recombination signal-binding protein; KBF2; NY REN 30 antigen; RBP J kappa; RBP-J; RBP-J kappa; RBP-JK; Rbpj; RBPJK; RBPSUH; Recombining binding protein suppressor of hairless; Renal carcinoma antigen NY-REN-30; SUH_HUMAN.
    产品应用WB=1:500-2000, IHC-P=1:100-500, IHC-F=1:100-500

    Not yet tested in other applications.
    Optimal working dilutions must be determined by the end user.

    抗体来源Rabbit
    免疫原KLH conjugated synthetic peptide derived from human RBPJK
    亚型IgG
    纯化方法affinity purified by Protein A
    克隆类型Polyclonal
    浓度1mg/ml
    储存液0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
    研究领域

    Epigenetics and Nuclear Signaling > Transcription > Other factors

    Epigenetics and Nuclear Signaling > Transcription > Transcription Factors

    Stem Cells > Signaling Pathways > Notch > Nuclear

    亚基Interacts with activated NOTCH1, NOTCH2 or NOTCH3. Interacts with MINT/SHARP. This interaction may mediate the recruitment of large corepressor complexes containing proteins such as HDAC1, HDAC2, NCOR2, SAP30, FHL1/KYOT2 and CIR1. Interacts with EP300, MAML1 and PTF1A. Interacts with Epstein-Barr virus EBNA2, EBNA3, EBNA4 and EBNA6. Interacts with RITA/C12orf52, leading to nuclear export, prevent the interaction between RBPJ and NICD product and subsequent down-regulation of the Notch signaling pathway. Interacts with SNW1.
    亚细胞定位Nucleus. Cytoplasm. Note=Mainly nuclear, upon interaction with RITA/C12orf52, translocates to the cytoplasm, down-regulating the Notch signaling pathway.
    相似性Belongs to the Su(H) family.
    Contains 1 IPT/TIG domain.
    功能Transcriptional regulator that plays a central role in Notch signaling, a signaling pathway involved in cell-cell communication that regulates a broad spectrum of cell-fate determinations. Acts as a transcriptional repressor when it is not associated with Notch proteins. When associated with some NICD product of Notch proteins (Notch intracellular domain), it acts as a transcriptional activator that activates transcription of Notch target genes. Probably represses or activates transcription via the recruitment of chromatin remodeling complexes containing histone deacetylase or histone acetylase proteins, respectively. Specifically binds to the immunoglobulin kappa-type J segment recombination signal sequence. Binds specifically to methylated DNA.
    保存条件Shipped at 4℃. Store at -20°C for one year. Avoid repeated freeze/thaw cycles.
    注意事项This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
    背景资料Transcriptional regulator that plays a central role in Notch signaling, a signaling pathway involved in cell-cell communication that regulates a broad spectrum of cell-fate determinations. Acts as a transcriptional repressor when it is not associated with Notch proteins. When associated with some NICD product of Notch proteins (Notch intracellular domain), it acts as a transcriptional activator that activates transcription of Notch target genes. Probably represses or activates transcription via the recruitment of chromatin remodeling complexes containing histone deacetylase or histone acetylase proteins, respectively. Specifically binds to the immunoglobulin kappa-type J segment recombination signal sequence.

     

    应用推荐稀释比例
    {WB}{1:500-2000}
    {IHC-P}{1:100-500}
    {IHC-F}{1:100-500}

     

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    图标文献和实验
    相关实验
    • Western 杂交

      SDS-PA gels, and subsequent detection of proteins using rabbit antisera and alkaline phosphatase-conjugated goat-anti-rabbit IgG, detected using bromo-chloro-indolyl phosphate (BCIP) and Nitro-blue tetrazolium (NBT) salts.    ・        

    • Developing Genetically Engineered Mouse Models to Study Tumor Suppression

      Literature Cited    Armstrong, J.F., Kaufman, M.H., Harrison, D.J., and Clarke, A.R. 1995. High‐frequency developmental abnormalities in p53‐deficient mice. Curr

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