PERK (D11A8) Rabbit mAb

PERK (D11A8) Rabbit mAb

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  • 询价
  • Cell Signaling Technology已认证
  • USA
  • 2025年11月13日
  • W, IP, IHC-P
  • H
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    • 详细信息
    • 技术资料
    • 抗体英文名

      PERK (D11A8) Rabbit mAb

    • 抗原

      synthetic peptide corresponding to residues surrounding Leu156 of human PERK protein

    • 应用范围

      W, IP, IHC-P

    • 保质期

      详见说明书

    • 供应商

      CST

    • 级别

      详见MSDS文件

    • 适应物种

      H

    • 库存

      大量

    • 是否单克隆

      1

    • 保存条件

      -20°c

    • 规格

      40 ul (4 western blots)/100 ul (10 western blots)/carrier free & custom formulation / quantity

    规格:产品价格:¥请询价
    规格:40 ul (4 western blots)产品价格:¥请询价
    规格:100 ul (10 western blots)产品价格:¥请询价
    规格:carrier free & custom formulation / quantity产品价格:¥请询价

    pathway more info application references datasheet PDF MSDS PDF protocols

    Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IHC-P=Immunohistochemistry (Paraffin)
    Reactivity Key:  H=Human
    Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

    Applications Reactivity Sensitivity MW (kDa) Isotype
    W IP IHC-P H Endogenous 140 Rabbit IgG
    Protocols
    Specificity / Sensitivity

    PERK (D11A8) Rabbit mAb recognizes endogenous levels of total PERK protein. Staining of red blood cells has been observed. The specificity of this staining is unknown.

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu156 of human PERK protein.

    Western Blotting

    Western Blotting

    Western blot analysis of extracts from various cell lines using PERK (D11A8) Rabbit mAb.

    IHC-P (paraffin)

    IHC-P (paraffin)

    Immunohistochemical analysis of paraffin-embedded human breast carcinoma using PERK (D11A8) Rabbit mAb.

    Background

    PERK (protein kinase-like endoplasmic reticulum kinase) is an eIF2α kinase and transmembrane protein resident in the endoplasmic reticulum (ER) membrane that couples ER stress signals to translation inhibition (1-3). ER stress increases the activity of PERK, which then phosphorylates eIF2α to promote reduced translation. PERK-deficient mice have defects in pancreatic β cells several weeks after birth, suggesting a role for PERK-mediated translational control in protecting secretory cells from ER stress (4). PERK activation during ER stress correlates with autophosphorylation of its cytoplasmic kinase domain (1-3). Phosphorylation of PERK at Thr980 serves as a marker for its activation status.

    1. Harding, H. et al. (1999) Nature 397, 271-274.
    2. Shi, Y. et al. (1998) Mol. Cell. Biol. 18, 7499-7509.
    3. Harding, H. et al. (2000) Mol. Cell 5, 897-904.
    4. Harding, H. et al. (2001) Mol. Cell 7, 1153-1163.
    Application References

    Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know !

    Companion Products

    For Research Use Only. Not For Use In Diagnostic Procedures.

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