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RSPH6A Rabbit pAb, AP conjugat

ed(bs-18875R-AP)-100ul
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  • ¥2980
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  • bs-18875R-AP
  • 2025年09月30日
  • 产品信息以Bioss网站为准
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      100ul

    产品编号bs-18875R-AP
    英文名称RSPH6A Rabbit pAb, AP conjugated
    中文名称AP标记的RSPH6A蛋白抗体
    英文别名Ortholog of mouse radial spokehead like 1; Radial spoke head 6 homolog A(Chlamydomonas); Radial spoke head protein 6 homolog A; Radial spoke head-like protein 1; Radial spokehead-like 1; RSH6A_HUMAN; RSHL1; RSP4; RSP6; RSPH4B; rsph6a.
    产品应用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 RSPH6A
    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.
    相似性Belongs to the flagellar radial spoke RSP4/6 family.
    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The protein encoded by this gene is similar to a sea urchin radial spoke head protein. Radial spoke protein complexes form part of the axoneme of eukaryotic flagella and are located between the axoneme's outer ring of doublet microtubules and central pair of microtubules. In Chlamydomonas, radial spoke proteins are thought to regulate the activity of dynein and the symmetry of flagellar bending patterns. This gene maps to a region of chromosome 19 that is linked to primary ciliary dyskinesia-2 (CILD2). [provided by RefSeq, Jul 2008]

     

    应用推荐稀释比例
    {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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