Cell Signaling Technology

Product Pathways - Adhesion

GIT-1 Antibody #2919

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R Hm Mk B Endogenous 95 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  Hm=Hamster  Mk=Monkey  B=Bovine
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

GIT-1 Antibody recognizes endogenous levels of total GIT-1 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human GIT-1. Antibodies are purified using peptide affinity chromatography.

Western Blotting

Western Blotting

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

IP

IP

Immunoprecipitation of GIT-1 from CHO cells using GIT-1 Antibody. Western blot detection was performed using the same antibody.

Background

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).

  1. Hoefen, R.J. and Berk, B.C. (2006) J. Cell Sci. 119, 1469-1475.
  2. Manabe, R. et al. (2002) J. Cell Sci. 115, 1497-1510.
  3. Zhang, H. et al. (2003) J. Cell Biol. 161, 131-142.
  4. Goehler, H. et al. (2004) Mol. Cell 15, 853-865.
  5. Mende-Mueller, L.M. et al. (2001) J. Neurosci. 21, 1830-1837.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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