Cell Signaling Technology

Product Pathways - Development

LEF1 (C12A5) Rabbit mAb #2230

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP IF-IC F H M R Endogenous 25-58 kDa Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IF-IC=Immunofluorescence (Immunocytochemistry)  F=Flow Cytometry
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

LEF1 (C12A5) Rabbit mAb detects endogenous level of total LEF1 protein. It does not recognize the dominant negative forms of LEF1 generated by an alternative promoter.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro82 of human LEF1.

Western Blotting

Western Blotting

Western blot analysis of total cell lysates from HCT15, DLD1 and mouse thymocytes using LEF1 (C12A5) Rabbit mAb.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of untreated Jurkat cells using LEF1 (C12A5) Rabbit mAb (blue) compared to a nonspecific negative control antibody (red).

IF-IC

IF-IC

Confocal immunofluorescent analysis of HCT-15 cells using LEF1 (C12A5) Rabbit mAb (green) and Pan-Keratin (C11) Mouse mAb #4545 (red).


Background

LEF1 and TCF are members of the high mobility group (HMG) DNA binding protein family of transcription factors that consists of the following: Lymphoid Enhancer Factor 1 (LEF1), T Cell Factor 1 (TCF1), TCF3, and TCF4 (1). LEF1 and TCF1 were originally identified as important factors regulating early lymphoid development (2) and act downstream in Wnt signaling. LEF1 and TCF bind to Wnt response elements to provide docking sites for β-catenin, which translocates to the nucleus to promote the transcription of target genes upon activation of Wnt signaling (3). LEF1 and TCF are dynamically expressed during development and aberrant activation of the Wnt signaling pathway is involved in many types of cancers including colon cancer (4,5).

LEF1 has several isoforms due to alternative splicing. LEF1 also has an alternative promoter that is preferentially active in lymphocytes. The isoforms generated by this alternative promoter have no amino-terminal β-catenin binding domain and may function in a dominant negative manner (6-8).

  1. Waterman, M.L. (2004) Cancer Metastasis Rev. 23, 41-52.
  2. Schilham, M.W. and Clevers, H. (1998) Semin. Immunol. 10, 127-132.
  3. Brantjes, H. et al. (2002) Biol. Chem. 383, 255-261.
  4. Reya, T. and Clevers, H. (2005) Nature 434, 843-850.
  5. Logan, C.Y. and Nusse, R. (2004) Annu. Rev. Cell Dev. Biol. 20, 781-810.
  6. Hovanes, K. et al. (2000) Nucleic Acids Res. 28, 1994-2003.
  7. Hovanes, K. et al. (2001) Nat. Genet. 28, 53-57.
  8. Kobielak, A. et al. (2001) Acta. Biochim. Pol. 48, 221-226.

Application References

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

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