Home Primary Antibodies Phospho-NF-κB p65 (Ser529) Antibody [F5A1]

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Phospho-NF-κB p65 (Ser529) Antibody [F5A1]

Cat.No.: F4238

    Application: Reactivity:
    • F4238-wb
      Lane 1: THP-1 (TPA, 50 ng/mL，18 h; rested 48 h), Lane 2: THP-1 (TPA, 50 ng/mL，18 h; rested 48 h; LPS, 5 μg/mL，15 min)

    Usage Information

    Dilution
    1:1000
    1:50
    1:3200
    1:100-1:400
    Application
    WB, IP, IF, FCM
    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
    65 kDa

    Datasheet & SDS

    Biological Description

    Specificity
    Phospho-NF-κB p65 (Ser529) Antibody [F5A1] detects endogenous levels of total NF-κB p65 protein only when it is phosphorylated at Ser529.
    Clone
    F5A1
    Synonym(s)
    Transcription factor p65; Nuclear factor NF-kappa-B p65 subunit; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3; RELA; NFKB3
    Background
    Phospho-NF-κB p65 at Ser529 (p65-S529ph) is a post-translational modification of the transcriptionally active p65 subunit within the canonical NF-κB pathway, modulating DNA-binding affinity, promoter engagement, and gene transcription. In resting cells, p65 is sequestered in the cytoplasm by IκB proteins. Upon cytokine stimulation (e.g., TNF-α), the IKK complex phosphorylates and degrades IκB, freeing p65-containing dimers for nuclear translocation and binding to κB-motif promoters of genes controlling inflammation, cell survival, and immunity. Ser529 phosphorylation, mediated by casein kinase II and related kinases after IκB dissociation, occurs within the p65 transactivation domain. While this modification does not impede nuclear entry, it enhances p65’s ability to recruit coactivators and chromatin-modifying complexes, thereby amplifying transcriptional activation of NF-κB-dependent pro-inflammatory and anti-apoptotic genes. P65-S529ph signaling contributes to cytokine-driven endothelial activation, macrophage polarization, and T- and B-cell immune responses, making this modification a valuable readout for NF-κB pathway engagement in both innate and adaptive immunity. Dysregulation of Ser529 phosphorylation in chronic inflammation and cancer leads to persistent NF-κB activity, resistance to apoptosis, and pro-tumorigenic signaling, implicating aberrant p65-S529ph in various inflammatory and oncogenic diseases.
    References
    • https://pubmed.ncbi.nlm.nih.gov/25862606/
    • https://pubmed.ncbi.nlm.nih.gov/30464573/

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