Anti-Aurora B (phospho Y12)抗体(ab62466)

概述

  • 产品名称Anti-Aurora B (phospho Y12)抗体
    参阅全部 Aurora B 一抗
  • 描述
    兔多克隆抗体to Aurora B (phospho Y12)
  • 特异性ab62466 detects endogenous levels of Aurora B only when phosphorylated at tyrosine 12.
  • 经测试应用适用于: ELISA, IHC-Pmore details
  • 种属反应性
    与反应: Human
    预测可用于: Mouse, Rat
  • 免疫原

    Synthetic phosphopeptide derived from human Aurora B around the phosphorylation site of tyrosine 12 (W-P-YP-G-R).

  • 阳性对照
    • Human liver carcinoma.

性能

应用

Our Abpromise guarantee covers the use of ab62466 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

应用 Ab评论 说明
ELISA 1/10000.
IHC-P 1/50 - 1/100.

靶标

  • 功能May be directly involved in regulating the cleavage of polar spindle microtubules and is a key regulator for the onset of cytokinesis during mitosis. Component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis. The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly. Phosphorylates 'Ser-10' and 'Ser-28' of histone H3 during mitosis. Required for kinetochore localization of BUB1 and SGOL1. Interacts with INCENP.
  • 组织特异性High level expression seen in the thymus. It is also expressed in the spleen, lung, testis, colon, placenta and fetal liver. Expressed during S and G2/M phase and expression is up-regulated in cancer cells during M phase.
  • 疾病相关Note=Disruptive regulation of expression is a possibile mechanism of the perturbation of chromosomal integrity in cancer cells through its dominant-negative effect on cytokinesis.
  • 序列相似性Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. Aurora subfamily.
    Contains 1 protein kinase domain.
  • 翻译后修饰Ubiquitinated by different BCR (BTB-CUL3-RBX1) E3 ubiquitin ligase complexes. Ubiquitinated by the BCR(KLHL9-KLHL13) E3 ubiquitin ligase complex, ubiquitination leads to removal from mitotic chromosomes and is required for cytokinesis. During anaphase, the BCR(KLHL21) E3 ubiquitin ligase complex recruits the CPC complex from chromosomes to the spindle midzone and mediates the ubiquitination of AURKB. Ubiquitination of AURKB by BCR(KLHL21) E3 ubiquitin ligase complex may not lead to its degradation by the proteasome.
  • 细胞定位Nucleus. Chromosome. Chromosome > centromere. Cytoplasm > cytoskeleton > spindle. Localizes on chromosome arms and inner centromeres from prophase through metaphase and then transferring to the spindle midzone and midbody from anaphase through cytokinesis. Colocalized with gamma tubulin in the mid-body.
  • Information by UniProt
  • 数据库链接
  • 别名
    • AIK2 antibody
    • AIM-1 antibody
    • AIM1 antibody
    • ARK-2 antibody
    • ARK2 antibody
    • AurB antibody
    • AURKB antibody
    • AURKB_HUMAN antibody
    • Aurora 1 antibody
    • Aurora and Ipl1 like midbody associated protein 1 antibody
    • Aurora kinase B antibody
    • Aurora related kinase 2 antibody
    • Aurora- and Ipl1-like midbody-associated protein 1 antibody
    • Aurora-B antibody
    • Aurora-related kinase 2 antibody
    • Aurora/IPL1 related kinase 2 antibody
    • Aurora/IPL1-related kinase 2 antibody
    • IPL1 antibody
    • PPP1R48 antibody
    • Protein phosphatase 1 regulatory subunit 48 antibody
    • Serine/theronine kinase 12 antibody
    • Serine/threonine protein kinase 12 antibody
    • Serine/threonine-protein kinase 12 antibody
    • Serine/threonine-protein kinase aurora-B antibody
    • STK-1 antibody
    • STK1 antibody
    • STK12 antibody
    • STK5 antibody
    see all

Anti-Aurora B (phospho Y12) antibody 图像

  • ab62466, at 1/50 dilution, staining Aurora B in human liver carcinoma tissue by Immunohistochemsitry in the absence (left image) or presence (right image) of the immunising peptide.

Anti-Aurora B (phospho Y12) antibody (ab62466)参考文献

ab62466 has not yet been referenced specifically in any publications.

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