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LRRK2 (E7P4V) Mouse mAb (BSA and Azide Free)

LRRK2 (E7P4V) Mouse mAb (BSA and Azide Free) #80846

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ELISA

Supporting Data

REACTIVITY	H M
SENSITIVITY	Endogenous
MW (kDa)	290
Source/Isotype	Mouse IgG2b kappa

Application Key:

ELISA-ELISA

Species Cross-Reactivity Key:

H-Human
M-Mouse

Product Information

Product Usage Information

This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.

BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.

Formulation

Supplied in 1X PBS (10 mM Na₂HPO₄, 3 mM KCl, 2 mM KH₂PO₄, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.

Storage

Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.

Specificity / Sensitivity

LRRK2 (E7P4V) Mouse mAb (BSA and Azide Free) detects endogenous levels of LRRK2 protein. Mouse cross-reactivity determined by ELISA.

Species Reactivity:

Human, Mouse

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthethic peptide corresponding to residues surrounding Leu1840 of human LRRK2.

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 hallmarks of PD are 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). Research studies have shown various genes and loci are genetically linked to PD including α-synuclein/PARK1 and 4, parkin/PARK2, UCH-L1/PARK5, PINK1/PARK6, DJ-1/PARK7, LRRK2/PARK8, synphilin-1, and NR4A2 (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. Research studies have linked at least 20 LRRK2 mutations to PD, with the G2019S mutation being the most prevalent (3). The G2019S mutation causes increased LRRK2 kinase activity, which induces a progressive reduction in neurite length that leads to progressive neurite loss and decreased neuronal survival (4). Researchers are currently testing the MLK inhibitor CEP-1347 in PD clinical trials, indicating the potential value of LRRK2 as a therapeutic target for treatment of PD (5).

Database Links

UniProt ID: Q5S007

Entrez-Gene Id: 120892

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

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