Render Target: STATIC
Render Timestamp: 2024-11-06T10:16:01.580Z
Commit: 642d75590e907c0f7dfc7c6e3b846bcc0b02197c
XML generation date: 2024-08-01 15:28:53.433
Product last modified at: 2024-09-05T16:45:07.697Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-LRRK2 (Ser935) Antibody #59576

Filter:
  • WB

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Transfected Only
    MW (kDa) 290
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Phospho-LRRK2 (Ser935) Antibody recognizes transfected levels of LRRK2 protein only when phosphorylated at Ser935.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser935 of human LRRK2 protein. Antibodies are purified by peptide affinity chromatography.

    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).
    Phosphorylation of LRRK2 at Ser910 and Ser935 plays a role in regulating interactions with 14-3-3 protein isoforms. Dephosphorylation of LRRK2 at these sites results in alerted subcellular localization and disrupted interactions with 14-3-3, events notably linked to the presence of five of the six most pathogenic LRRK2 mutations (R1441C, R1441G, R1441H, Y1699C, and I2020T) (6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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