AP-2α (C83E10) Rabbit mAb

• 产品编号：CST-3215S      品牌：CST       原厂货号：3215S
• 产品分类：抗体 > 一抗 > 蛋白特异性一抗
• 应用分类：

描述：

AP-2α (C83E10) Rabbit mAb 兔单抗能够检测内源 AP-2α 总蛋白。该单克隆抗体是通过合成人源AP-2α对应的多肽来免疫动物而获得。序列特异的转录因子激活蛋白2α (AP-2α)是哺乳动物发育过程中正常生长和形态形成所必需的(1,2)。在人类很多类型的癌症中，包括乳腺癌(3,4)、卵巢癌（5）、黑色素瘤（6）与前列腺癌(7)，研究已经发现AP-2α的降低或缺失表达。这些发现表明，AP-2α的表达在肿瘤发生过程中发挥了重要的作用。研究也发现，p53在人类乳腺癌细胞中的过表达能诱导AP-2α的表达。另外，p53结合到AP-2α启动子的cis-调控元件上, 表明AP-2α 是p53的靶标之一。 AP-2α可能具有介导p53抑制细胞增殖的功能(8)。

1. Mitchell, P.J. et al. (1987) Cell 50, 847-61.
2. Williams, T. and Tjian, R. (1991) Genes Dev 5, 670-82.
3. Douglas, D.B. et al. (2004) Cancer Res 64, 1611-20.
4. Gee, J.M. et al. (1999) J Pathol 189, 514-20.
5. Anttila, M.A. et al. (2000) Br J Cancer 82, 1974-83.
6. Jean, D. et al. (1998) J Biol Chem 273, 16501-8.
7. Ruiz, M. et al. (2004) Cancer Res 64, 631-8.
8. Li, H. et al. (2006) Oncogene 25, 5405-15.

原厂资料：

Specificity / Sensitivity

AP-2α (C83E10) Rabbit mAb detects endogenous levels of total AP-2α protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to human AP-2α.

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).

1. Mitchell, P.J. et al. (1987) Cell 50, 847-61.
2. Williams, T. and Tjian, R. (1991) Genes Dev 5, 670-82.
3. Douglas, D.B. et al. (2004) Cancer Res 64, 1611-20.
4. Gee, J.M. et al. (1999) J Pathol 189, 514-20.
5. Anttila, M.A. et al. (2000) Br J Cancer 82, 1974-83.
6. Jean, D. et al. (1998) J Biol Chem 273, 16501-8.
7. Ruiz, M. et al. (2004) Cancer Res 64, 631-8.
8. Li, H. et al. (2006) Oncogene 25, 5405-15.

注意事项：

1. Mitchell, P.J. et al. (1987) Cell 50, 847-61.
2. Williams, T. and Tjian, R. (1991) Genes Dev 5, 670-82.
3. Douglas, D.B. et al. (2004) Cancer Res 64, 1611-20.
4. Gee, J.M. et al. (1999) J Pathol 189, 514-20.
5. Anttila, M.A. et al. (2000) Br J Cancer 82, 1974-83.
6. Jean, D. et al. (1998) J Biol Chem 273, 16501-8.
7. Ruiz, M. et al. (2004) Cancer Res 64, 631-8.
8. Li, H. et al. (2006) Oncogene 25, 5405-15.