| 货号 | 4606S |
| 反应种属 | Human |
| 来源宿主 | Rabbit |
| 应用 | W |
| 目标/特异性 | TrkB Antibody detects transfected levels of total TrkB protein. |
| 使用方法 | WB(1:1000) |
| 供应商 | CST |
| 灵敏度 | Transfected Only |
| 背景 | 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).The phosphorylation sites are conserved between TrkA and TrkB: Tyr490 of TrkA corresponds to Tyr512 in TrkB, and Tyr674/675 of TrkA to Tyr706/707 in TrkB of the human sequence (7). TrkB is overexpressed in tumors such as neuroblastoma, prostate adenocarcinoma and pancreatic ductal adenocarcinoma. In neuroblastomas overexpression of TrkB correlates with unfavorable disease outcome when autocrine loops signaling tumor survival are potentiated by additional overexpression of brain-derived neurotrophic factor (BDNF). An alternatively spliced truncated TrkB isoform lacking the kinase domain is overexpressed in Wilms’s tumors and this isoform may act as a dominant-negative to TrkB signaling (8). |
| 存放说明 | -20C |
| 计算分子量 | 140 |
| 参考文献 | 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. 14 . Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8. 15 . Geiger, T.R. and Peeper, D.S. (2005) Cancer Res 65, 7033-6. 16 . Han, L. et al. (2007) Med Hypotheses 68, 407-9. 17 . Aoyama, M. et al. (2001) Cancer Lett 164, 51-60. 18 . Desmet, C.J. and Peeper, D.S. (2006) Cell Mol Life Sci 63, 755-9. |
Western blot analysis of extracts from NIH/3T3, NIH/3T3-TrkA, NIH/3T3-TrkB and NIH/3T3-TrkC cells, using TrkB Antibody (upper), TrkA Antibody #2505 (middle) and PLCγ1 Antibody #2822 (lower).对NIH/3T3、NIH/3T3-TrkA、NIH/3T3-TrkB和NIH/3T3-TrkC细胞抽提液使用TrkB抗体（上图）、TrkA抗体#2505（中图）和PLC-γ-1抗体#2822（下图）进行Western blot分析。 |
