research use only

Phospho-Tau (Ser422) Antibody [L19H1]

Cat.No.: F2605

    Application: Reactivity:

    Usage Information

    Dilution
    1:10000 - 1:20000
    Application
    WB
    Reactivity
    Human
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    50-100 kDa 55 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.
    Positive Control IMR-32 cells; SH-SY5Y cells (Okadiac acid and calyculin A treated)
    Negative Control SH-SY5Y cells; IMR-32 (phosphatase treated)

    Datasheet & SDS

    Biological Description

    Specificity
    Phospho-Tau (Ser422) Antibody [L19H1] detects endogenous levels of total Tau protein only when it is phosphorylated at Ser422.
    Clone
    L19H1
    Synonym(s)
    MAPT; Microtubule-associated protein tau; Neurofibrillary tangle protein; Paired helical filament-tau; PHF-tau
    Background
    Phospho-Tau (Ser422) is a disease-associated post-translational modification of the microtubule-associated protein Tau (MAPT), one of six brain isoforms (~352–441 aa) that normally stabilizes axonal microtubules via its N-terminal projection domain, proline-rich region (P1/P2 motifs), four microtubule-binding repeats (R1–R4), and C-terminal tail. Ser422 resides in the R2 repeat flanking the KXGS motifs critical for tubulin binding; phosphorylation at pSer422 (mimicked by S422E pseudophosphorylation) enhances SDS-stable dimer formation, prolongs aggregation nucleation, exposes the phosphatase-activating domain (PAD, aa 2-18), and alters tau conformers without changing total aggregate yield. pSer422 tau monomers inhibit anterograde kinesin-1-dependent fast axonal transport (FAT), while its aggregates uniquely block both anterograde and retrograde FAT, unlike unmodified tau, disrupting axonal trafficking of vesicles, mitochondria, and signaling molecules essential for neuronal viability. This modification correlates with cognitive decline, neuropil threads, and oligomeric tau in prodromal Alzheimer's disease (AD) brain, activating PP1-GSK3β pathways that exacerbate microtubule disassembly, synaptic loss, and neurodegeneration in tauopathies.
    References
    • https://pubmed.ncbi.nlm.nih.gov/27373205/
    • https://pubmed.ncbi.nlm.nih.gov/22690349/

    Tech Support

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3

    If you have any other enquiries, please leave a message.