R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
GIT2 (D11B8) Rabbit mAb #8072
Filter:
- WB
Supporting Data
| REACTIVITY | H M Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 85 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
GIT2 (D11B8) Rabbit mAb recognizes endogenous levels of total GIT2 protein.
Species Reactivity:
Human, Mouse, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human GIT2 protein.
Background
G protein-coupled receptor (GPCR) kinase interacting proteins 1 and 2 (GIT1 and GIT2) 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). GIT1 and GIT2 share many of the same properties, but with at least ten distinct, tissue-specific splice variants. GIT2 has been shown to play an important role inhibiting focal adhesion turnover and membrane protrusion (2,3). Focal adhesion localization and paxillin binding of GIT2 is regulated through phosphorylation at one or more tyrosine sites (Tyr286, Tyr392, Tyr592) by FAK and/or Src (4,5,reviewed in 6). Once at the focal adhesion, GIT2 is thought to play a key role in cell polarity and migration, making it a protein of interest in the investigation of oncogenic signaling pathways (3,5,7).
- Hoefen, R.J. and Berk, B.C. (2006) J Cell Sci 119, 1469-75.
- Premont, R.T. et al. (2000) J Biol Chem 275, 22373-80.
- Frank, S.R. et al. (2006) EMBO J 25, 1848-59.
- Brown, M.C. et al. (2005) Mol Biol Cell 16, 4316-28.
- Yu, J.A. et al. (2009) Mol Biol Cell 20, 4706-19.
- Yu, J.A. et al. (2010) Cell Adh Migr 4, 342-7.
- Mazaki, Y. et al. (2006) Nat Immunol 7, 724-31.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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