Cell Signaling Technology

Product Pathways - Neuroscience

LRRK2 Antibody #5559

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R Endogenous 290 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
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

LRRK2 Antibody detects endogenous levels of total LRRK2 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu1848 of human LRRK2 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse LRRK2-/- and wild-type tissue using LRRK2 Antibody (upper) and TrkB (80E3) Rabbit mAb #4603 (lower). (Mouse wild-type and LRRK2-/- brains were kindly provided by Dr. Jie Shen, Brigham and Women's Hospital and Harvard Medical School, Boston, MA).

Background

Parkinson’s disease (PD), the second most common neurodegenerative disease after Alzheimer’s, is a progressive movement disorder characterized by rigidity, tremors, and postural instability. The pathological hallmark of PD is progressive loss of dopaminergic neurons in the substantia nigra of the ventral midbrain and the presence of intracellular Lewy bodies (protein aggregates of α-synuclein, ubiquitin, and other components) in surviving neurons of the brain stem (1). Various genes and loci (α-synuclein/PARK1 and 4, parkin/PARK2, UCH-L1/PARK5, PINK1/PARK6, DJ-1/PARK7, LRRK2/PARK8, synphilin-1, and NR4A2) are genetically linked to PD (2).Leucine-rich repeat kinase 2 (LRRK2) contains amino-terminal leucine-rich repeats (LRR), a Ras-like small GTP binding protein-like (ROC) domain, an MLK protein kinase domain, and a carboxy-terminal WD40 repeat domain. At least 20 LRRK2 mutations have been linked to PD-the G2019S mutation being the most prevalent (3). The G2019S mutation causes increased LRRK2 kinase activity, which induces a progressive reduction in neurite length, leading to progressive neurite loss and decreased neuronal survival (4). The MLK inhibitor CEP-1347 is being tested in PD clinical trials, indicating the potential value of LRRK2 as a therapeutic target for treatment of PD (5).

  1. Fahn, S. (2003) Ann. NY Acad. Sci. 991, 1-14.
  2. Moore, D.J. et al. (2005) Annu. Rev. Neurosci. 28, 57-87.
  3. Mata, I.F. et al. (2006) Trends Neurosci. 29, 286-293.
  4. MacLeod, D. et al. (2006) Neuron 52, 587-593.
  5. Parkinson Study Group. (2004) Neurology 62, 330-332.

Application References

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Companion Products

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

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