Cell Signaling Technology

Product Pathways - Cytoskeletal Signaling

PAR2 (D61D5) Rabbit mAb #6976

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 32 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

PAR2 (D61D5) Rabbit mAb recognizes endogenous levels of total PAR2 protein. The major band detected runs at 32 kDa, the higher molecular weight smear is due to glycosylation.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly44 of human PAR2 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from HCT 116 and Hep G2 cells using PAR2 (D61D5) Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from COS-7 cells, untransfected (-) or transfected with human PAR2 (+), using PAR2 (D61D5) Rabbit mAb.

Background

PAR2 (F2RL1) belongs to the PAR (Protease-activated Receptor) family of G protein-coupled receptors. These membrane receptors are activated through N-terminal cleavage of the receptor by a serine protease such as thrombin, trypsin, or matrix metalloproteinases (1,2). This cleavage exposes the ‘tethered-ligand’ fragment of the receptor, which binds to a second extracellular loop of the receptor and leads to receptor activation. PAR2 is specifically activated by trypsin or trypsin-like proteases. Activated PAR2 stimulates phosphoinositide hydrolysis and calcium mobilization, interacts with β-arrestin, and eventually leads to ERK activation (3). PAR2 expression and activation are mainly associated with inflammatory diseases (3), but may also play a role in cancer development (4,5).

  1. Macfarlane, S.R. et al. (2001) Pharmacol Rev 53, 245-82.
  2. Ossovskaya, V.S. and Bunnett, N.W. (2004) Physiol Rev 84, 579-621.
  3. Bushell, T. (2007) J Physiol 581, 7-16.
  4. Su, S. et al. (2009) Oncogene 28, 3047-57.
  5. Gessler, F. et al. (2010) Neuroscience 165, 1312-22.

Application References

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

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