Product Pathways - Apoptosis / Autophagy
AP-2α Antibody #3208
| Applications | Reactivity | MW (kDa) | Source |
|---|---|---|---|
| W IP IHC-P IF-IC | H M R Mk | 48 | Rabbit |
Applications Key:
W=Western Blotting
IP=Immunoprecipitation
IHC-P=Immunohistochemistry (Paraffin)
IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:
H=Human
M=Mouse
R=Rat
Mk=Monkey
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.
Specificity / Sensitivity
AP-2α Antibody detects endogenous levels of total AP-2α protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide (KLH-coupled) derived from a sequence of human AP-2α. Antibodies are purified by protein A and peptide affinity chromatography.
IHC-P (paraffin)
Immunohistochemical analysis of paraffin-embedded human colon carcinoma, using AP-2alpha Antibody.
IHC-P (paraffin)
Immunohistochemical analysis of paraffin-embedded human lung carcinoma, using AP-2alpha Antibody.
Background
The sequence-specific transcription factor activator protein 2α (AP-2α) is required for normal growth and morphogenesis during mammalian development (1,2). Decreased or loss of AP-2α expression has been observed in many different types of human cancers including breast cancer (3,4), ovarian cancer (5), melanoma (6) and prostate cancer (7). These findings suggest that AP-2α expression plays a crucial role in tumorigenicity. Studies have also shown that p53 overexpression in human breast carcinoma cells induces the level of AP-2α expression. Furthermore, p53 binds to the cis-element in the AP-2α promoter, suggesting that AP-2α is a target of p53. AP-2α may mediate the effect of p53 to inhibit cell proliferation (8).
- Mitchell, P.J. et al. (1987) Cell 50, 847-61.
- Williams, T. and Tjian, R. (1991) Genes Dev 5, 670-82.
- Douglas, D.B. et al. (2004) Cancer Res 64, 1611-20.
- Gee, J.M. et al. (1999) J Pathol 189, 514-20.
- Anttila, M.A. et al. (2000) Br J Cancer 82, 1974-83.
- Jean, D. et al. (1998) J Biol Chem 273, 16501-8.
- Ruiz, M. et al. (2004) Cancer Res 64, 631-8.
- Li, H. et al. (2006) Oncogene 25, 5405-15.
Application References
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