Neuroscience
TrkB Antibody
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イイネ！(1)
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| CSTコード |
包装 |
希望納入価格 (円) |
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| #4606S | 100 μL | 46,000 | |
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TrkB抗体製品一覧
4606 の推奨プロトコール
最適な結果を得るために：Cell Signaling Technology (CST) 社は、各製品の推奨プロトコールを使用することを強くお薦めいたします。
推奨プロトコールはCST社内試験の徹底的なバリデーションに基づいて作成されておりますので、正確かつ再現性の高い結果が得られます。
注：各製品に最適化されたプロトコールをリンクしています。
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4606:
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Western Blotting
| 用途 (希釈倍率) | |
| ウェスタンブロッティング (1:1,000) |
| 特異性・感度 | |
| トランスフェクトレベルのTrkB タンパク質を検出します。 |
| 使用抗原 | |
| ヒトのTrkB タンパク質由来の配列 (合成ペプチド) |
Western Blotting
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).
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).
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Pierotti, M.A. and Greco, A. (2006) Cancer Lett 232, 90-8.
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Segal, R.A. and Greenberg, M.E. (1996) Annu Rev Neurosci 19, 463-89.
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Stephens, R.M. et al. (1994) Neuron 12, 691-705.
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Obermeier, A. et al. (1993) EMBO J 12, 933-41.
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Obermeier, A. et al. (1994) EMBO J 13, 1585-90.
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Yao, R. and Cooper, G.M. (1995) Science 267, 2003-6.
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Pierotti, M.A. and Greco, A. (2006) Cancer Lett. 232, 90-98.
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Huang, E.J. and Reichardt, L.F. (2003) Annu. Rev. Biochem. 72, 609-42.
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Desmet, C.J. and Peeper, D.S. (2006) Cell Mol. Life Sci. 63, 755-759.
PhosphoSitePlus®：
TrkB