research use only

GFI1 Antibody [M16D23]

Cat.No.: F7802

    Application: Reactivity:
    • F7802-wb
      Lane 1: THP-1, Lane 2: HL-60, Lane 3: Jurkat

    Usage Information

    Dilution
    1:1000
    1:100
    1:800-1:3200
    1:800-1:1600
    Application
    WB, IP, IF, FCM
    Reactivity
    Human, Mouse
    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
    55 kDa

    Datasheet & SDS

    Biological Description

    Specificity
    GFI1 Antibody [M16D23] detects endogenous levels of total GFI1 protein.
    Clone
    M16D23
    Synonym(s)
    Zinc finger protein Gfi-1; Growth factor independent protein 1; GFI1
    Background
    GFI1 functions as a transcriptional repressor within the growth factor independence 1 family alongside GFI1B, playing essential roles in hematopoietic development and differentiation. The protein contains an N-terminal SNAG domain that recruits corepressor complexes such as CoREST, LSD1, and HDAC1/2 to enforce gene silencing through chromatin modifications. GFI1 binds target promoters via zinc-finger motifs, suppressing proliferation genes in hematopoietic stem cells while promoting lineage commitment in lymphoid and myeloid progenitors. Interaction with RUNX1/ETO fusion sustains leukemia maintenance by stabilizing oncogenic transcription networks, where GFI1 loss impairs leukemia initiation and progression through disrupted epigenetic repression. In Group 3 medulloblastoma, enhancer hijacking elevates GFI1 expression adjacent to super-enhancers, cooperating with MYC amplification to drive tumor formation via mutually exclusive activation patterns with GFI1B. This positions GFI1 at regulatory hubs integrating proliferation control, differentiation blocks, and oncogenic signaling in neural and blood lineages. Dysregulated high expression correlates with poor prognosis in acute myeloid leukemia subtypes bearing NPM1 mutations or FLT3-ITD, while variant alleles like S36N accelerate disease through altered repressor function.
    References
    • https://pubmed.ncbi.nlm.nih.gov/25043047/
    • https://pubmed.ncbi.nlm.nih.gov/29674496/

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