Mig6 Antibody

Mig6 Antibody

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  • 询价
  • Cell Signaling Technology已认证
  • USA
  • 2025年12月02日
  • W
  • Rabbit
  • H
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    • 详细信息
    • 技术资料
    • 抗体英文名

      Mig6 Antibody

    • 抗原

      synthetic peptide corresponding to residues surrounding Val195 of human Mig6

    • 应用范围

      W

    • 宿主

      Rabbit

    • 级别

      详见MSDS文件

    • 库存

      大量

    • 供应商

      CST

    • 适应物种

      H

    • 保质期

      详见说明书

    • 是否单克隆

      2

    • 保存条件

      -20°c

    • 规格

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

    规格: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
    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) Source
    W H Endogenous 51 Rabbit
    Protocols
    Specificity / Sensitivity

    Mig6 Antibody detects endogenous levels of total Mig6 protein.

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val195 of human Mig6. Antibodies are purified by protein A and peptide affinity chromatography.

    Western Blotting

    Western Blotting

    Western blot analysis of extracts from HepG2 and HCT116 cells using Mig6 Antibody.

    Background

    Mig6 was identified as a gene which is induced when quiescent fibroblasts are treated by mitogens (1). During cell cycle progression, Mig6 expression levels are also regulated (1). Mig6 mRNA levels were found to increase upon stimulation by chronic stresses including diabetic nephropathy (2). Overexpression of this gene leads to the activation of stress-activated protein kinases (SAPKs)/c-Jun amino-terminal kinases (JNKs) (2). Furthermore, Mig6 was found to interact with epidermal growth factor receptor (EGFR) when stimulated by epidermal growth factor (EGF) (3). Deletion of the Mig6 gene in mice results in hyperactivation of EGFR and signaling through the mitogen-activated protein kinase (MAPK) pathway, causing overproliferation and abnormal differentiation of epidermal keratinocytes in these animals. Inhibition of endogenous EGFR signaling by Iressa abolished skin defects observed in Mig6(-/-) mice, indicating that Mig6 is a specfic negative regulator of EGFR signaling (4). Furthermore, expression of Mig6 was significantly lower in skin, breast, pancreatic and ovarian cancers, suggesting a role of Mig6 as a tumor suppressor (4).

    1. Wick, M. et al. (1995) Exp. Cell Res. 219, 527-535.
    2. Makkinje, A. et al. (2000) J. Biol. Chem. 275, 17838-17847.
    3. Hackel, P.O. et al. (2001) Biol. Chem. 382, 1649-1662.
    4. Ferby, I. et al. (2006) Nat. Med. 12, 568-573.
    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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