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IKZF3 Antibody [D19G22]

Cat.No.: F4871

    Application: Reactivity:
    • F4871-wb
      Lane 1: Raji, Lane 2: Ramos, Lane 3: Jurkat

    Usage Information

    Dilution
    1:20000
    1:50 - 1:100
    1:100
    1:10 - 1:100
    Application
    WB, IHC, IF, 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
    58 kDa 70 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 Human spleen tissue; Mouse cardiac muscle tissue; Rat spleen tissue; Human thymus cells; Jurkat cells; Raji cells; Ramos cells
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    IKZF3 Antibody [D19G22] detects endogenous levels of total IKZF3 protein.
    Clone
    D19G22
    Synonym(s)
    ZNFN1A3; IKZF3; Zinc finger protein Aiolos; Ikaros family zinc finger protein 3
    Background
    IKZF3 (Aiolos) is a hematopoietic-specific zinc finger transcription factor from the Ikaros family, essential for B-cell development and effector maturation. It contains an N-terminal DNA-binding domain with four tandem C2H2 zinc fingers that recognize the core GGAAA motif, particularly through major groove contacts made by key arginine and histidine residues, and a C-terminal dimerization domain with two additional zinc fingers that enable homo- and heterodimerization with other Ikaros proteins such as IKZF1 (Ikaros), IKZF2 (Helios), and IKZF4 (Eos), facilitating both repressive and activating transcriptional complexes. IKZF3 orchestrates sequential B-cell programming: initial IKZF1 homodimers establish lymphoid priming, while IKZF1:IKZF3 heterodimers recruit chromatin remodeling and co-repressor complexes such as NuRD, SWI/SNF, and PRC2 to silence pro-apoptotic genes and enforce survival checkpoints. As B cells mature, IKZF3 homodimers activate key regulators like BLIMP1, STAT3, and XBP1 to drive plasma cell differentiation and antibody secretion. In regulatory T cells, IKZF3 modulates IL-10 expression indirectly through synergy with FOXP3. Germline dominant-negative IKZF3 variants can interfere with IKZF1 function, repressing genes involved in B and T cell homing and leading to immunodeficiency, while somatic overexpression of IKZF3 sustains aberrant BCR and IL-7R signaling in leukemias.
    References
    • https://pubmed.ncbi.nlm.nih.gov/38216003/
    • https://pubmed.ncbi.nlm.nih.gov/37662955/

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