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JunD (D17G2) Rabbit mAb

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  • 询价
  • Cell Signaling Technology已认证
  • USA
  • 2026年01月02日
  • W, IP, IF-IC, F
  • H,Mk,B,Pg
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    • 详细信息
    • 文献和实验
    • 技术资料
    • 抗体英文名

      JunD (D17G2) Rabbit mAb

    • 抗原

      synthetic peptide corresponding to residues surrounding Pro250 of human JunD protein

    • 应用范围

      W, IP, IF-IC, F

    • 库存

      大量

    • 保质期

      详见说明书

    • 适应物种

      H,Mk,B,Pg

    • 供应商

      CST

    • 级别

      详见MSDS文件

    • 是否单克隆

      1

    • 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  IP=Immunoprecipitation  IF-IC=Immunofluorescence (Immunocytochemistry)  F=Flow Cytometry
    Reactivity Key:  H=Human  Mk=Monkey  B=Bovine  Pg=Pig
    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 IF-IC F H Mk B Pg Endogenous 38, 42 Rabbit IgG
    Protocols
    Specificity / Sensitivity

    JunD (D17G2) Rabbit mAb recognizes endogenous levels of total JunD protein. This antibody is not predicted to cross-react with other Fos/Jun family members.

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro250 of human JunD protein.

    Western Blotting

    Western Blotting

    Western blot analysis of extracts from various cell lines using JunD (D17G2) Rabbit mAb.

    Flow Cytometry

    Flow Cytometry

    Flow cytometric analysis of HeLa cells using JunD (D17G2) Rabbit mAb (blue) compared to concentration-matched Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (red).

    IF-IC

    IF-IC

    Confocal immunofluorescent analysis of HeLa cells using JunD (D17G2) Rabbit mAb (green). Actin filaments were labeled with DY-554 phalloidin (red).


    Background

    JunD, along with closely related family members c-Jun and JunB, is a transcription factor that can activate or repress a wide array of target genes (1,2). JunD transcriptional activity is modulated by phosphorylation in response to cellular stress via the c-Jun N-terminal Kinase (JNK)/Stress-Activated Protein Kinase (SAPK) family of protein kinases (3,4). JunD activity can also be modulated by the MAPK pathway in response to growth factors. Its transcriptional capacity is further regulated by other binding partners that affect JunD expression levels and DNA binding capacity (reviewed in 5). All Jun proteins are capable of forming dimers with Fos-, ATF- and CREB-family transcription factors to form the AP-1 complex that differentially regulates a variety of target genes involved in cellular growth, proliferation, differentiation, and apoptosis (reviewed in 5 and 6). Unlike JunB and c-Jun, which share a high degree of homology (>95%), JunD is less conserved (~75%) at the amino acid level (1). Growing evidence suggests that JunD protein expression is regulated independently of other family members (reviewed in 5). It is thought that JunD may have functional significance beyond the typical Jun-family milieu. This is exemplified by the fact that JunD knockout mice are viable, bearing specific defects in cardiomyocyte function and bone growth, whereas their c-Jun counterparts develop significant, multi-organ defects during embryogenesis and die at E12.5 (7-10). JunD appears to specifically regulate genes involved in antioxidant response and hydrogen peroxide production and plays an important role in angiogenesis via its ability to exert transcriptional control over the VEGF gene (11). Furthermore, JunD appears to play an important roll in metabolism via modulation of IGF-I signaling pathways (12). Recent studies have shown that JunD regulates GADD45 α and γ expression in prostate cancer cells and that inhibition of JunD promotes apoptosis. Thus, JunD may be a viable therapeutic target for the treatment of prostate cancer (13).

    1. Berger, I. and Shaul, Y. (1991) Oncogene 6, 561-6.
    2. Hernandez, J.M. et al. (2008) Oncogene 27, 4757-67.
    3. Vinciguerra, M. et al. (2004) J Biol Chem 279, 9634-41.
    4. Stocco, C.O. et al. (2002) J Biol Chem 277, 3293-302.
    5. Hernandez, J.M. et al. (2008) Oncogene 27, 4757-67.
    6. Eferl, R. and Wagner, E.F. (2003) Nat Rev Cancer 3, 859-68.
    7. Thépot, D. et al. (2000) Development 127, 143-53.
    8. Hilberg, F. et al. (1993) Nature 365, 179-81.
    9. Meixner, A. et al. (2010) Cell Death Differ 17, 1409-19.
    10. Hilfiker-Kleiner, D. et al. (2005) Circulation 112, 1470-7.
    11. Gerald, D. et al. (2004) Cell 118, 781-94.
    12. Laurent, G. et al. (2008) Cell Metab 7, 113-24.
    13. Zerbini, L.F. et al. (2011) Cell Cycle 10, 2583-91.
    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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