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Contributor Information

  • Name Helen Hurst
  • Institute Queen Mary University of London

Tool Details

  • Tool name: Anti-AP2 (a&b) [A6/2/2]
  • Clone: A6/2/2
  • Tool type: Antibodies
  • Tool sub-type: Primary antibody
  • Class: Monoclonal
  • Conjugate: Unconjugated
  • Reactivity: Human
  • Host: Mouse
  • Application: ELISA ; FACS ; IHC ; IF ; RIA ; WB
  • Description: AP-2 is a family of developmentally regulated transcription factors which also play a role in breast cancer and melanoma. AP-2?Ÿ may be important in cardiac and kidney development. The AP-2 transcription factors form the OB2 complex that has been shown to up-regulate c-erb-B2 transcription.
  • Immunogen: Peptide to C-Terminal of AP-2 Alpha coupled to KLH. PNSHTDNNAKSSDKEEKHRK
  • Isotype: IgG1
  • Research area: Cancer; Tissue-specific biology; Genetics
  • Myeloma used: NS0

  • For Research Use Only

Target Details

  • Target: Activating Protein 2 (AP-2) alpha and beta forms.
  • Target background: AP-2 is a family of developmentally regulated transcription factors which also play a role in breast cancer and melanoma. AP-2? may be important in cardiac and kidney development. The AP-2 transcription factors form the OB2 complex that has been shown to up-regulate c-erb-B2 transcription.

Application Details

  • Application: ELISA ; FACS ; IHC ; IF ; RIA ; WB

Handling

  • Format: Liquid
  • Concentration: 1 mg/ml
  • Storage buffer: PBS with 0.02% azide
  • Storage conditions: -15°C to -25°C
  • Shipping conditions: Shipping at 4°C

Documentation

References

  •   Yang et al. 2005. J Am Soc Nephrol. 16(10):2890-6. PMID: 16107581.
  •   Redistribution of myosin VI from top to base of proximal tubule microvilli during acute hypertension.
  •   Gee et al. 1999. J Pathol. 189(4):514-20. PMID: 10629551.
  •   Immunohistochemical analysis reveals a tumour suppressor-like role for the transcription factor AP-2 in invasive breast cancer.
  •   Batsch et al. 1998. Mol Cell Biol. 18(7):3647-58. PMID: 9632747.
  •   RB and c-Myc activate expression of the E-cadherin gene in epithelial cells through interaction with transcription factor AP-2.