TrkA (14G6) Rabbit mAb

• 产品编号：CST-2508P      品牌：Cell Signaling Technology       原厂货号：2508P
• 产品分类：抗体 > 一抗 > 蛋白特异性一抗
• 应用分类：

描述：

TrkA (14G6)Rabbit mAb 兔单抗识别内源性的TrkA总蛋白。此抗体与TrkB蛋白没有交叉反应。该单克隆抗体由合成的人TrkA蛋白Arg220位点附近肽段免疫动物而制成。

Trk受体酪氨酸激酶家族包括TrkA，TrkB和TrkC。这些家庭成员的序列是高度保守的，它们是由不同的神经营养因子激活：NGF激活TrkA，BDNF或NT4激活TrkB，NT3激活TrkC。TrkA调节细胞增殖，神经系统的发育和成熟很重要（1）。在Tyr490磷酸化，需要与Shc结合及Ras-MAP激酶级联的激活。Tyr674/675残基在催化域内，此位点的磷酸化能影响TrkA的激酶活性（2-6）。点突变，缺失和染色体重排（嵌合体）会引起配体依赖受体的二聚化，激活TrkA。许多恶性肿瘤，包括乳腺癌、结肠癌、前列腺癌、甲状腺癌和急性髓细胞白血病有激活的TrkA。神经母细胞瘤的TrkA表达是一个预后良好的指标，因为它标志着肿瘤生长停滞和从神经嵴分化而来（1）。

1. Huang, E.J. and Reichardt, L.F. (2003) Annu Rev Biochem 72, 609-42.
2. Segal, R.A. and Greenberg, M.E. (1996) Annu Rev Neurosci 19, 463-89.
3. Stephens, R.M. et al. (1994) Neuron 12, 691-705.
4. Marsh, H.N. et al. (2003) J Cell Biol 163, 999-1010.
5. Obermeier, A. et al. (1993) EMBO J 12, 933-41.
6. Obermeier, A. et al. (1994) EMBO J 13, 1585-90.
7. Arevalo, J.C. et al. (2001) Oncogene 20, 1229-34.
8. Reuther, G.W. et al. (2000) Mol Cell Biol 20, 8655-66.
9. Greco, A. et al. (1997) Genes Chromosomes Cancer 19, 112-23.
10. Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8.
11. Lagadec, C. et al. (2009) Oncogene 28, 1960-70.
12. Greco, A. et al. (2010) Mol Cell Endocrinol 321, 44-9.
13. Ødegaard, E. et al. (2007) Hum Pathol 38, 140-6.

原厂资料：

Specificity / Sensitivity

TrkA (14G6) Rabbit mAb detects endogenous levels of total TrkA protein. This antibody does not cross-react with TrkB.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide surrounding Arg220 of human TrkA.

Background

The family of Trk receptor tyrosine kinases consists of TrkA, TrkB and TrkC. While the sequence of these family members is highly conserved, they are activated by different neurotrophins: TrkA by NGF, TrkB by BDNF or NT4, and TrkC by NT3. TrkA regulates proliferation and is important for development and maturation of the nervous system (1). Phosphorylation at Tyr490 is required for Shc association and activation of the Ras-MAP kinase cascade. Residues Tyr674/675 lie within the catalytic domain, and phosphorylation at this site reflects TrkA kinase activity (2-6). Point mutations, deletions and chromosomal rearrangements (chimeras) cause ligand-independent receptor dimerization and activation of TrkA. Many malignancies including breast, colon, prostate and thyroid carcinomas and acute myeloid leukemia have activated TrkA. Expression of TrkA in neuroblastomas is a good prognostic marker because it signals growth arrest and differentiation of cells originating from the neural crest (1).

1. Huang, E.J. and Reichardt, L.F. (2003) Annu Rev Biochem 72, 609-42.
2. Segal, R.A. and Greenberg, M.E. (1996) Annu Rev Neurosci 19, 463-89.
3. Stephens, R.M. et al. (1994) Neuron 12, 691-705.
4. Marsh, H.N. et al. (2003) J Cell Biol 163, 999-1010.
5. Obermeier, A. et al. (1993) EMBO J 12, 933-41.
6. Obermeier, A. et al. (1994) EMBO J 13, 1585-90.
7. Arevalo, J.C. et al. (2001) Oncogene 20, 1229-34.
8. Reuther, G.W. et al. (2000) Mol Cell Biol 20, 8655-66.
9. Greco, A. et al. (1997) Genes Chromosomes Cancer 19, 112-23.
10. Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8.
11. Lagadec, C. et al. (2009) Oncogene 28, 1960-70.
12. Greco, A. et al. (2010) Mol Cell Endocrinol 321, 44-9.
13. Ødegaard, E. et al. (2007) Hum Pathol 38, 140-6.

注意事项：

Storage: Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM
NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C.
Do not aliquot the antibody