Ask about this productRelated genes to: GFI1 antibody
- 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
Related articles to: GFI1 antibody
- The immune system's evolution is crucial for its role in fighting pathogens and involvement in autoimmune and neurodegenerative diseases. The GFI1 gene family plays a role in the regulation of the function of immune cells, including neutrophils and CD4 + T cells. GFI1 consists of two members, GFI1A and GFI1B. GFI1A is vital for myeloid and lymphoid differentiation, while GFI1B is crucial for generating red blood cells and platelets. Both genes share a repressor SNAG domain and C2H2 zinc finger domains. However, the full relationship between their structure and function remains unclear. We aimed to decipher the relationship between structural evolution and novel functionalization in the GFI1 gene family. We employed a comprehensive phylogenetic approach that integrated tree construction, ancestral state reconstruction, positive selection analysis, motif mining, and non-homology-based functional prediction to trace GFI1 family evolutionary history over 700 million years. Our analysis revealed that the GFI1 gene family originated from a single ancestral gene in early metazoans and underwent multiple lineage-specific duplication events in invertebrates, jawless vertebrates, and jawed vertebrates, indicating adaptive diversification across evolutionary lineages, albeit without evidence of significant positive selection. We identified new motifs in the less-characterized middle regions, such as the SPOP-binding motif in GFI1A, potentially regulating cytokine production in CD4 + T cells, and the FEDFW motif, possibly involved in neutrophil recruitment. These motifs are unique to GFI1A in higher vertebrates. In GFI1B, we discovered a unique EPLRP motif, a separase cleavage site linked to sister chromatid separation. Our results indicate that GFI1 has evolved new functions to adapt to the complexity of the vertebrate immune system. - Source: PubMed
Publication date: 2026/04/28
Religa PiotrKubick NorwinŁazarczyk MarzenaTsegaye BiniyamŁawiński MichałPaszkiewicz JustynaAtanasov AtanasHorbańczuk JarosławSacharczuk MariuszMickael Michel - Natural killer cells defend against malignancies and viral infections through a tightly controlled program of differentiation and maturation. However, the transcriptional mechanisms guiding this process remain incompletely defined. Using paired single-cell multiomic profiling, we identify GFI1 as an epigenetic regulator of NK cell differentiation, coordinating EOMES and T-BET transcriptional balance to promote NK cell proliferation and the transition from immature to terminally differentiated NK cell states. GFI1 represses FOXO1 chromatin accessibility in mature NK cells, which normally limits NK cell proliferation and maturation. Co-deletion of both GFI1 and FOXO1 largely rescues NK cell differentiation, identifying a critical GFI1-FOXO1 axis required for protection against tumour metastasis. These findings position GFI1 as a key transcriptional node integrating NK cell differentiation, activation and effector programs. - Source: PubMed
Publication date: 2026/04/22
Huang QiutongChaudhry M ZeeshanDight JamesAlim LouisaYu HuiyangDenman RenaeMan Hiu OnSchreuder JaringGarnham Alexandra LTuong Zewen KSouza-Fonseca-Guimaraes FernandoJacquelot NicolasBelz Gabrielle T - 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