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RAD51D Rabbit pAb, AP conjugat

ed(bs-19726R-AP)-100ul
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  • ¥2980
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  • bs-19726R-AP
  • 2025年09月30日
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      100ul

    产品编号bs-19726R-AP
    英文名称RAD51D Rabbit pAb, AP conjugated
    中文名称AP标记的RAD51D蛋白抗体
    英文别名BROVCA4; DNA repair protein RAD51 homolog 4; HsTRAD; OTTHUMP00000163851; OTTHUMP00000163852; OTTHUMP00000163853; R51H3; RA51D_HUMAN; RAD51 homolog D(S. cerevisiae); RAD51 homolog D; RAD51 like 3(S. cerevisiae); RAD51 paralog D; RAD51, S. cerevisiae, homolog of, D; RAD51-like protein 3; Rad51l3; Recombination repair protein; S. cerevisiae RAD51-like 3; TRAD.
    产品应用WB=1:500-2000

    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 RAD51D
    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 > DNA / RNA > DNA Damage & Repair > Homologous Recomb.

    亚基Part of the BCDX2 complex consisting of RAD51B, RAD51C, RAD51D and XRCC2; the complex has a ring-like structure arranged into a flat disc around a central channel. In the absence of DNA, the BCDX2 subcomplex XRCC2:RAD51D formed a multimeric ring structure; in the presence of single-stranded DNA it formed a filamentous structure with the ssDNA. Interacts with SWSAP1 and ZSWIM7; involved in homologous recombination repair. Interacts with BLM; required for stimulation of BLM activity by the BCDX2 subcomplex XRCC2:RAD51D.
    亚细胞定位Nucleus.
    组织特异性Expressed in colon, prostate, spleen, testis, ovary, thymus and small intestine. Weakly expressed in leukocytes.
    相似性Belongs to the RecA family. RAD51 subfamily.
    功能Involved in the homologous recombination repair (HRR) pathway of double-stranded DNA breaks arising during DNA replication or induced by DNA-damaging agents. Bind to single-stranded DNA (ssDNA) and has DNA-dependent ATPase activity. Part of the Rad21 paralog protein complex BCDX2 which acts in the BRCA1-BRCA2-dependent HR pathway. Upon DNA damage, BCDX2 acts downstream of BRCA2 recruitment and upstream of RAD51 recruitment. BCDX2 binds predominantly to the intersection of the four duplex arms of the Holliday junction and to junction of replication forks. The BCDX2 complex was originally reported to bind single-stranded DNA, single-stranded gaps in duplex DNA and specifically to nicks in duplex DNA. Involved in telomere maintenance. The BCDX2 subcomplex XRCC2:RAD51D can stimulate Holliday junction resolution by BLM.
    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 a member of the RAD51 protein family. RAD51 family members are highly similar to bacterial RecA and Saccharomyces cerevisiae Rad51, which are known to be involved in the homologous recombination and repair of DNA. This protein forms a complex with several other members of the RAD51 family, including RAD51L1, RAD51L2, and XRCC2. The protein complex formed with this protein has been shown to catalyze homologous pairing between single- and double-stranded DNA, and is thought to play a role in the early stage of recombinational repair of DNA. Alternative splicing results in multiple transcript variants. Read-through transcription also exists between this gene and the downstream ring finger and FYVE-like domain containing 1 (RFFL) gene. [provided by RefSeq, Jan 2011]

     

    应用推荐稀释比例
    {WB}{1:500-2000}

     

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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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