Datasheet

生物学的記述

Specificity	GFI1 Antibody [M16D23] detects endogenous levels of total GFI1 protein.
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.

Specificity

GFI1 Antibody [M16D23] detects endogenous levels of total GFI1 protein.

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.

使用情報

Application

WB, IP, IF, FCM

Dilution

WB	IP	IF	FCM
1:1000	1:100	1:800-1:3200	1:800-1:1600

Reactivity

Human, Mouse

Source

Rabbit Monoclonal Antibody

MW

55 kDa

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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/25043047/
https://pubmed.ncbi.nlm.nih.gov/29674496/

Application Data

WB

Validated by Selleck

Lane 1: THP-1, Lane 2: HL-60, Lane 3: Jurkat