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Phospho-ErbB3/HER3 (Tyr1289) Antibody [P19F5]

Cat.No.: F3001

    Application: Reactivity:

    Usage Information

    Dilution
    1:2500 - 1:5000
    1:100
    Application
    WB, IF
    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
    148 kDa 185 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.

    Datasheet & SDS

    Biological Description

    Specificity
    Phospho-ErbB3/HER3 (Tyr1289) Antibody [P19F5] detects endogenous levels of total HER3/ErbB3 protein only when it is phosphorylated at Tyr1289.
    Clone
    P19F5
    Synonym(s)
    HER3; ERBB3; Receptor tyrosine-protein kinase erbB-3; Proto-oncogene-like protein c-ErbB-3; Tyrosine kinase-type cell surface receptor HER3
    Background
    Phospho-ErbB3/HER3 (Tyr1289), the tyrosine-phosphorylated form at residue 1289 of the kinase-impaired ErbB3 receptor (a 185 kDa member of the EGFR/ErbB family with an extracellular ligand-binding domain, single-span transmembrane helix, catalytically inactive juxtamembrane/intracellular kinase domain featuring a disrupted ATP-binding pocket, and a C-terminal tail harboring at least nine phospho-tyrosines including the YXXM motif at Tyr1289), emerges upon ligand-induced (neuregulin) heterodimerization with active ErbB partners like EGFR/ErbB1 or HER2/ErbB2, where the partner's kinase phosphorylates ErbB3 in trans, triggering a conformational shift that exposes the pTyr1289 docking site for the p85 regulatory subunit of PI3K to initiate robust PI3K/AKT/mTOR signaling for cell survival, proliferation, and migration, while also recruiting Grb2/Sos for parallel MAPK/ERK activation and Src family kinases for crosstalk, distinct from other sites like Tyr1222, pTyr1289 uniquely drives high-affinity PI3K binding due to its YXXM sequence, amplifying oncogenic signaling in heterodimers without ErbB3's own kinase activity. This phosphorylation sustains rapid receptor recycling/trafficking, sustains autocrine loops in tumors, and resists apoptosis, with overexpression/hyperactivation prevalent in breast, lung, ovarian, and head/neck cancers, where ErbB2-ErbB3 dimers fuel therapy resistance, invasion/metastasis via EMT, and poor prognosis.
    References
    • https://pubmed.ncbi.nlm.nih.gov/31351986/
    • https://pubmed.ncbi.nlm.nih.gov/22733765/

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