概述

  • 产品名称
    人FLASH肽

描述

  • 性质
    Synthetic
  • 氨基酸序列
    • 种属
      Human
    • 序列
      SERFQQLMKLFEKSKC Amino acids 1253 to 1268 of human FLASH (1).
    • 氨基酸
      1966 to 1981

相关产品

技术指标

Our Abpromise guarantee covers the use of ab8455 in the following tested applications.

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

  • 应用

    Blocking - Blocking peptide for Anti-FLASH antibody (ab8420)

    Western blot

  • 形式
    Liquid
  • Concentration information loading...

制备和贮存

  • 稳定性和存储

    Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.

    PBS with 0.1% BSA 0.02% sodium azide pH7.2

常规信息

  • 别名
    • AA387232
    • C8AP2_HUMAN
    • CASP 8 associated protein 2
    • CASP8 associated protein 2
    • CASP8-associated protein 2
    • CASP8AP2
    • Caspase 8 associated protein 2
    • CED 4
    • CED4
    • D4Ertd659e
    • FLASH homolog
    • FLASH homolog RIP 25
    • FLASH homolog RIP25
    • FLICE associated huge
    • FLICE associated huge protein
    • FLICE-associated huge protein
    • FLJ11208
    • KIAA1315
    • mKIAA1315
    • OTTMUSP00000005125
    • RIP 25
    • RIP25
    • RP23-69G24.1
    see all
  • 功能
    Participates in TNF-alpha-induced blockade of glucocorticoid receptor (GR) transactivation at the nuclear receptor coactivator level, upstream and independently of NF-kappa-B. Suppresses both NCOA2- and NCOA3-induced enhancement of GR transactivation. Involved in TNF-alpha-induced activation of NF-kappa-B via a TRAF2-dependent pathway. Acts as a downstream mediator for CASP8-induced activation of NF-kappa-B. Required for the activation of CASP8 in FAS-mediated apoptosis. Required for histone gene transcription and progression through S phase.
  • 翻译后修饰
    Phosphorylated upon DNA damage, probably by ATM or ATR.
  • 细胞定位
    Cytoplasm. Nucleus. Localizes to discrete nuclear foci.
  • Information by UniProt

文献

ab8455 has not yet been referenced specifically in any publications.

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