GFI1 antibody - N-terminal region (ARP31869_P050)
- Known as:
- GFI1 (anti-) - N-terminal region (ARP31869_P050)
- Catalog number:
- arp31869_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GFI1 antibody - N-terminal region (ARP31869_P050)
Related genes to: GFI1 antibody - N-terminal region (ARP31869_P050)
- Gene:
- GFI1 NIH gene
- Name:
- growth factor independent 1 transcriptional repressor
- Previous symbol:
- ZNF163
- Synonyms:
- GFI1A, GFI-1
- Chromosome:
- 1p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-10-17
- Date modifiied:
- 2019-04-23
Related products to: GFI1 antibody - N-terminal region (ARP31869_P050)
Related articles to: GFI1 antibody - N-terminal region (ARP31869_P050)
- Dysfunctional hematopoietic stem cells (HSC) drive the initiation of myelodysplastic syndromes (MDS), yet the genome-wide DNA methylation landscape of primitive MDS HSCs and its mechanistic contribution to disease pathogenesis remain poorly defined. Here, we establish single-base resolution DNA methylomes of bone marrow HSCs from MDS patients and healthy donors. We uncover the widespread hypermethylation in CpG islands, alongside hypomethylation in repetitive elements such as Alu. Differentially methylated regions are enriched for genes involved in cancer-related pathways, as well as extrinsic signaling pathways and intrinsic transcriptional networks essential for HSC function. Among these, we identify GFI1 and BMI1 as key targets of DNA methylation dysregulation in MDS. Notably, using either the MDS or a TET2-deficient mouse model, we demonstrate that loss of TET2, a frequently mutated epigenetic regulator in MDS, induces promoter hypermethylation and transcriptional repression of , contributing to the expansion of the MDS or aged hematopoietic stem and progenitor cell pool. Our study not only charts the base-resolution DNA methylome of human MDS HSCs but also reveals a TET2-GFI1 axis that safeguards HSC homeostasis. These findings provide mechanistic insight into how aberrant DNA methylation drives HSC dysfunction in MDS and offer an epigenomic resource for discovering regulators and therapeutic targets at the stem cell level. - Source: PubMed
Publication date: 2026/04/01
Hu LiangdingShen QicongGu YanLu JiahuiLi YuhangLiu NaZhang BinHan YanmeiZhang QianCao Xuetao - Research in 2025 demonstrated that memory and exhausted CD8 T cell lineages arise from shared TCF1 progenitors and that fate divergence is actively enforced by transcriptional programs rather than fixed at priming. Multi-state regulators such as KLF2 and GFI1 preserve stemness, restrain exhaustion, and calibrate differentiation under acute and chronic antigenic stress. - Source: PubMed
Publication date: 2026/03/11
Chaudhry M ZeeshanBelz Gabrielle T - Ribosomal DNA copy number (rDNAcn) and DNA methylation are important modulators of the human genome, both studied in relation to overall cellular function, biological ageing, and disease development. Despite the overlapping roles, their relationship remains poorly understood, especially in the early stages of life, characterized by rapid growth and high cellular demands. Even though previous studies have associated rDNA methylation with cancer and ageing, no study to date has examined the interplay between rDNAcn and whole-genome DNA methylation. In an epigenome-wide association study of 45S rDNAcn variation in 194 newborns, we show strong positive associations between rDNAcn and single DNA methylated CpGs, measured with the Illumina EPIC array. Out of the 122 Bonferroni-significant CpGs, 63.5% were also Bonferroni-significant in a replication cohort of 167 newborns, in which a second EWAS was conducted using DNA methylation data from the Illumina 450K array. The identified CpGs were dispersed over the autosomes and were not functionally related to the rDNA-forming nucleolar-associated domains. The top CpGs were annotated to genes (, , , ) that are functionally linked to cancer and cellular proliferation. In downstream analyses, the 122 rDNAcn-related CpGs revealed 31 differentially methylated regions and 253 nominally significant correlations with cord blood gene transcripts in an eQTM analysis. Pathway enrichment analyses showed an overrepresentation of the following pathways: 'RNA Polymerase III transcription' (R-HSA-76071, R-HSA-76046, R-HSA-74158, R-HSA-749476, R-HSA-73780, R-HSA-73980, R-HSA-76066, R-HSA-76061, hsa03020), 'cytosolic sensors of pathogen-associated DNA' (R-HSA-1834949), 'RNA polymerase II transcribes snRNA genes' (R-HSA-6807505), and 'translation initiation' (R-HSA-72613, R-HSA-72737). Our findings reveal a close link between rDNAcn variation and DNA methylation in early life. Disruptions in this interplay may influence cellular functions critical for early development, potentially shaping health and disease trajectories later in life. - Source: PubMed
Publication date: 2026/03/03
Barth KathrinAlfano RossellaPlusquin MichelleWang CongrongNawrot Tim SMartens Dries S - Durable control of HIV infection is challenged by persistent latent reservoirs, including hematopoietic stem and progenitor cells (HSPCs), which provide a unique niche for proviral silencing. Mechanisms of HIV latency in HSPCs remain poorly studied. Here, we utilized a dual-reporter HIV (89.6 VT1) and single-cell RNA sequencing to identify host factors governing latency in HSPCs. Transcriptomic profiling revealed elevated expression of several genes in latently infected cells, among them the transcriptional repressor GFI1. Functional studies showed that GFI1 suppresses HIV gene expression by binding a conserved sequence near the primer binding site within the long terminal repeat (LTR). Disruption of GFI1 DNA-binding or corepressor recruitment domains diminished its silencing effect. GFI1 also antagonized Tat and NF-κB-mediated activation, and reversal of GFI1-mediated suppression was most robust with combined HDAC inhibition and NF-κB activation. These findings position GFI1 as an important regulator of HIV latency in HSPCs. - Source: PubMed
Publication date: 2026/02/20
Onyango Jackline ALi ChenChen CuieDisbennett W MiguelVirgilio Maria CPainter Mark MTerry Valeri HRamnani BarkhaWelch Joshua DCollins Kathleen L - CD8 T cells differentiate into diverse states that shape immune outcomes in cancer and chronic infection. To define systematically the transcription factors (TFs) driving these states, we built a comprehensive atlas integrating transcriptional and epigenetic data across nine CD8 T cell states and inferred TF activity profiles. Our analysis catalogued TF activity fingerprints, uncovering regulatory mechanisms governing selective cell state differentiation. Leveraging this platform, we focused on two transcriptionally similar but functionally opposing states that are critical in tumour and viral contexts: terminally exhausted T (TEX) cells, which are dysfunctional, and tissue-resident memory T (T) cells, which are protective. Global TF community analysis revealed distinct biological pathways and TF-driven networks underlying protective versus dysfunctional states. Through in vivo CRISPR screening integrated with single-cell RNA sequencing (in vivo Perturb-seq) we delineated several TFs that selectively govern TEX cell differentiation. We also identified HIC1 and GFI1 as shared regulators of TEX and T cell differentiation and KLF6 as a unique regulator of T cells. We discovered new TEX-selective TFs, including ZSCAN20 and JDP2, with no previous known function in T cells. Targeted deletion of these TFs enhanced tumour control and synergized with immune checkpoint blockade but did not interfere with T cell formation. Consistently, their depletion in human T cells reduces the expression of inhibitory receptors and improves effector function. By decoupling exhaustion T-selective from protective T cell programmes, our platform enables more precise engineering of T cell states, accelerating the rational design of more effective cellular immunotherapies. - Source: PubMed
Publication date: 2026/02/04
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