Neuroscience
GIT-1 Antibody
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| CSTコード |
包装 |
希望納入価格 (円) |
国内在庫  |
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| #2919S | 100 μL | 46,000 | |
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GIT1抗体製品一覧
2919 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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2919:
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Immunoprecipitation
Western Blotting
| 用途(希釈倍率) | |
| ウエスタンブロッティング(1:1,000)、免疫沈降(1:100) |
| 特異性・感度 | |
| 内在性レベルのGIT-1 タンパク質の検出します。 |
| 使用抗原 | |
| ヒトのGIT-1 タンパク質のC末端近傍領域(合成ペプチド) |
Western Blotting

Western blot analysis of extracts from various cell types using GIT-1 Antibody.
IP

Immunoprecipitation of GIT-1 from CHO cells using GIT-1 Antibody. Western blot detection was performed using the same antibody.
G-protein coupled receptor (GPCR) kinase interacting proteins 1 and 2 (GIT-1 and GIT-2) are highly conserved, ubiquitous scaffold proteins involved in localized signaling to help regulate focal contact assembly and cytoskeletal dynamics. GIT proteins contain multiple interaction domains that allow interaction with small GTPases (including ARF, Rac and cdc42), kinases (such as PAK and MEK), the Rho family GEF PIX, and the focal adhesion protein paxillin (reviewed in 1). GIT-1 is localized to focal adhesions, cytoplasmic complexes and membrane protrusions, and regulates cell protrusion formation and cell migration (2). GIT-1 has also been implicated in neuronal functions including synapse formation (3) and the pathology of Huntington disease (4). Huntington disease is a genetic neurodegenerative condition involving a mutation in the huntington gene. The huntington gene product (htt) is ubiquitinated and degraded in human Huntington disease brains (5). Htt interacts directly with GIT-1 causing enhanced htt proteolysis, indicating that GIT-1 distribution and function may contribute to Huntington disease pathology (4).
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Hoefen, R.J. and Berk, B.C. (2006) J. Cell Sci. 119, 1469-1475.
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Manabe, R. et al. (2002) J. Cell Sci. 115, 1497-1510.
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Zhang, H. et al. (2003) J. Cell Biol. 161, 131-142.
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Goehler, H. et al. (2004) Mol. Cell 15, 853-865.
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Mende-Mueller, L.M. et al. (2001) J. Neurosci. 21, 1830-1837.