CST, 26880SF, LRRK2 (D18E12) Rabbit Monoclonal Antibody (BSA and Azide Free)

Monoclonal Antibody for studying LRRK2. Validated for Western Blotting,ELISA+. Highly specific and rigorously validated in-house, LRRK2 (D18E12) Rabbit Monoclonal Antibody (BSA and Azide Free) (CST #26880) is ready to ship. Product Usage Information This product is the carrier free version of product #13046. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol. 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 Na 2 HPO 4 , 3 mM KCl, 2 mM KH 2 PO 4 , and 140 mM NaCl (pH 7.8)). BSA and Azide Free. For standard formulation of this product see product # 13046 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 (D18E12) Rabbit Monoclonal Antibody (BSA and Azide Free) recognizes endogenous levels of total LRRK2 protein. Species Reactivity: Human, Mouse, Rat Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro2080 of human LRRK2 protein. 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). Alternate Names augmented in rheumatoid arthritis 17; AURA17; Dardarin; leucine rich repeat kinase 2; leucine-rich repeat kinase 2; Leucine-rich repeat serine/threonine-protein kinase 2; LRRK2; PARK8; RIPK7; ROCO2 Specification REACTIVITY: H M R SENSITIVITY: Endogenous MW (kDa): 290 Source/Isotype: Rabbit IgG