Cell Signaling Technology

Product Pathways - Neuroscience

mGluR1 (D5H10) Rabbit mAb #12551

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP IF-F H M R Endogenous 145, >300 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IF-F=Immunofluorescence (Frozen)
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

mGluR1 (D5H10) Rabbit mAb recognizes endogenous levels of total mGluR1 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu1105 of human mGluR1 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from neonatal mouse brain and rat brain using mGluR1 (D5H10) Rabbit mAb.

IF-F

IF-F

Confocal immunofluorescent analysis of adult mouse cerebellum tissue using mGluR1 (D5H10) Rabbit mAb (green). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).

Background

Metabotropic glutamate receptor 1 (mGluR1) is a G protein-coupled receptor (GPCR) for the neurotransmitter glutamate in the mammalian brain. Unlike ionotropic receptors, metabotropic receptors do not form an ion channel pore themselves but are indirectly linked to ion channels (1). Both mGluR1 and mGluR5 are coupled to phospholipase C and activate inositol phospholipid metabolism via G protein-mediated mechanisms. Upon phosphatidylinositol activation, the second messenger calcium is released and generates a calcium-activated chloride current. Metabotropic glutamate receptors other than mGluR1 and mGluR5 inhibit adenylate cyclase (1-3). mGluR1 does not share sequence homology with conventional GPCRs (1). mGluR1 forms a homodimer and is linked to synaptic plasticity, as well as long-term potentiation and long-term depression. Furthermore, mGluR1 is a potential therapeutic target for various psychiatric and neurological diseases, including schizophrenia, epilepsy, and Parkinson and Alzheimer diseases (4-6).

  1. Pin, J.P. et al. (1994) EMBO J 13, 342-8.
  2. Sugiyama, H. et al. (1987) Nature 325, 531-3.
  3. Hermans, E. and Challiss, R.A. (2001) Biochem J 359, 465-84.
  4. Niswender, C.M. et al. (2005) Curr Top Med Chem 5, 847-57.
  5. Pellicciari, R. and Costantino, G. (1999) Curr Opin Chem Biol 3, 433-40.
  6. Olive, M.F. (2009) Curr Drug Abuse Rev 2, 83-989.

Application References

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Companion Products

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

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