Home Primary Antibodies Phospho-Src (Tyr419) Antibody [D21H6]

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Phospho-Src (Tyr419) Antibody [D21H6]

Cat.No.: F2480

    Application: Reactivity:
    • F2480-wb
      Lane 1: A431, Lane 2: A431 (Pervanadate, 50 mM, 5 min), Lane 3: NIH/3T3, Lane 4: NIH/3T3 (Pervanadate, 50 mM, 5 min)

    Usage Information

    Dilution
    1:5000
    1:100
    Application
    WB, FCM
    Reactivity
    Mouse, Rat, 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
    60 kDa 60 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.
    Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

    Datasheet & SDS

    Biological Description

    Specificity
    Phospho-Src (Tyr419) Antibody [D21H6] detects endogenous levels of total Src protein only when it is phosphorylated at Tyr419.
    Clone
    D21H6
    Synonym(s)
    SRC1; SRC; Proto-oncogene tyrosine-protein kinase Src; Proto-oncogene c-Src; pp60c-src; p60-Src
    Background
    Phospho-Src (Tyr419), the activation loop phosphorylation marking full catalytic competence of the Src family kinase prototype, unlocks bidirectional tyrosine kinase signaling from virtually all integrin, growth factor, and GPCR stimuli across adherent cells and platelets. Dephosphorylation of inhibitory Tyr530 by CD45/PTP1B relieves SH2 domain clamping, permitting trans-autophosphorylation at Tyr419 that rigidly positions the activation loop for substrate access while relieving steric occlusion of the ATP-binding cleft; this catalyzes hierarchical phosphorylation cascades where Src primes receptor tyrosine kinases through Y1009/1101 autophosphorylation on EGFR while amplifying FAK at Y397/576/577/861 to scaffold paxillin/PI3K recruitment. Active p-Tyr419-Src drives Ras-GRF1/ERK for proliferation, STAT3/5a for survival, and cortactin/pyk2 for invadopodia maturation via sequential Arp2/3 activation; feedback engages Csk/Shp1 through C-terminal docking to restore Tyr530 phosphorylation, while PP2A/PP1 dephosphorylate the activation loop for signal termination. In platelets, shear-induced clustering at podosome-like adhesions generates local p-Tyr419 gradients that license αIIbβ3 outside-in signaling for clot retraction, while fibroblasts exploit Src for durotaxis through myosin-IIA/Y1183 feedback with tension sensors.
    References
    • https://pubmed.ncbi.nlm.nih.gov/9988270/
    • https://pubmed.ncbi.nlm.nih.gov/23923048/

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