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
- To understand the role of gambogic acid in regulating apoptosis in Raji cells, experiments were performed to examine the signaling pathways. The study was carried out using a cell growth inhibition assay to detect the activity changes of Raji cells, as well as analyzing the regulatory process of apoptosis and regulatory genes through the cell apoptosis assay. To detect the changes in regulatory genes of Raji cells after treatment, experimental groups with different doses and concentrations of gambogic acid were assigned. The interference experiment was designed to investigate the regulatory mechanism of gambogic acid on the apoptosis process of Raji cells. The experiments with dose-response showed that gambogic acid achieved the highest inhibition of cell proliferation at concentrations of 0-2 µM. The treatment duration of 12-24 h was identified as the optimal treatment. In apoptosis assays (24 h), total apoptotic rates increased to 13.28% ± 0.52%, 22.55% ± 0.71%, and 40.52% ± 1.02% following gambogic acid treatment at 0.25, 0.5, 1.0 µg/mL respectively, compared with 4.98% ± 0.19% in the control group (p < 0.05). The expression of the Gfi-1 (Growth Factor Independent 1) gene was suppressed in gambogic acid-treated cells (p < 0.05), while gambogic acid markedly upregulated the apoptotic protein cleaved caspase-3. These findings suggest that Gambogic acid inhibits the STAT5 pathway by regulating the Gfi-1 gene through promoting apoptosis in Raji cells. Therefore, the anti-cancer mechanism of gambogic acid on Raji cells is influenced by the STAT5 pathway. - Source: PubMed
Publication date: 2026/08/25
Ruan JunZhou JingmeiXu QinLiu XiaoqianXiong LingfanShu Xiaoyan - GFI1 is a DNA-binding transcription factor that regulates the commitment of hematopoietic precursors to myeloid and lymphoid lineages. Here we report that GFI1 is expressed in γδ T cells and restricts the cellularity of RORγtVγ6 γδ T cells that produce high levels of IL-17A while promoting the expansion of Vγ1 and Vγ4 γδ T cells. GFI1 deficiency results in an expansion of Vγ6 γδT17 cells that starts post-birth and is strongly exacerbated upon challenge with an inflammatory allergen. Additionally, we observe an expansion of RORγt/MAF cells within the thymic DN1e population of GFI1-deficient mice. The DN1e population, along with other DN subsets in GFI1-deficient mice, exhibits a distinctive γδT17 cell-specific transcriptomic profile. Specifically, DN1, DN3, and γδ T cells lacking GFI1 show upregulation of the B-ZIP transcription factor MAF, which regulates genes critical for γδ T cells, such as , , and . The gene is occupied by GFI1 in DN pre-T cells at cognate binding sites in its promoter region, suggesting that GFI1 acts as a direct repressor of . We conclude that GFI1 functions as a novel regulator of Vγ6 γδT17 precursor cells restricting their peripheral expansion by acting upstream of a MAF-dependent regulatory network. - Source: PubMed
Publication date: 2026/08/05
Fraszczak JenniferObwegs DavidArman KaifeeMuralt TanjaThurairajah BavanithaMallet Gauthier ÈveKing Irah LMelichar Heather JSagar Möröy Tarik - Vestibular hair cells (HCs) are sensory mechanotransducers essential for balance and spatial orientation, yet the relative contributions of HC number and subtype to vestibular function remain unresolved. Here, we developed a dose-dependent injury model in adult Pou4f3 mice by administering diphtheria toxin (DT), which induced selective HC ablation across vestibular organs. Both type I and type II HCs were lost following DT treatment. Type II HCs exhibited higher susceptibility to DT at lower doses, although this difference diminished as DT dose increased and overall HC survival declined. Functional analyses revealed that mice retaining ~ 30% of vestibular HCs-with preserved subtype proportions and neural innervation-exhibited normal balance, while ~ 50% residual HCs were sufficient to maintain intact vestibulo-ocular reflexes. To elucidate subtype-specific roles, we employed two type I HC-deficient models: 3,3'-iminodipropionitrile-induced injury and Gfi1/Atoh1-OE mice. Comparative analyses revealed that type I HCs were essential for vestibular function. Together, these findings establish a reliable injury model, demonstrate functional redundancy within vestibular HCs, and underscore the critical role of type I HCs. These insights suggest that efforts to restore vestibular function through HC regeneration should prioritize generating functional type I HCs, not merely increasing the total HC count. - Source: PubMed
Publication date: 2026/07/17
Huang YikangNi WenliZhou QinFeng MingchuanJiang TaoHe ShunjiChen YanLi Wenyan - Retinal direction selectivity is a vital component of many visual functions, including motion processing and gaze stabilization. Direction selectivity emerges from specialized retinal ganglion cells (RGCs) that encode motion along a single preferred direction. In the mouse retina, direction-selective (DS) RGC (DSGC) subtypes are quite diverse, but little is known about the genetic programs required to generate this diversity. Moreover, it is unclear whether transcription factors that specify distinct DS subtypes play additional roles in their maintenance or maturation. Here, we show that the transcription factor Gfi1 is a conserved regulator of two DSGC subtypes tuned to vertical motion: down ON-type DSGCs (D-oDSGCs) and F-mini ONs. We show that Gfi1 promotes early differentiation of both subtypes but has distinct roles later in their development. In D-oDSGCs, Gfi1 is required postnatally for directing dendritic elaboration, and loss of Gfi1 disrupts D-oDSGC-mediated downward motion-tracking behavior, whereas in F-mini ONs, Gfi1 is required for continued cell survival . These findings reveal shared and divergent temporally segregated functions of Gfi1 in the assembly of retinal DS circuits. - Source: PubMed
Publication date: 2026/07/13
Chaudhari KarinaGuzman-Clavel Luis EDonthi NityaYang JeffreyHarris Scott CLin Tzu-HuaiDunn Felice AKolodkin Alex L - Macrophages are versatile immune cells, with the ability to respond to varied intrinsic and extrinsic cues and transition between inflammatory and proreparative phenotypes. A complex network of epigenetic processes, such as DNA methylation, histone methylation, and acetylation, plays key roles in modulating macrophage polarization and inflammatory gene expression. Transcriptional analysis in patients with respiratory failure, long COVID-19, and influenza revealed an augmented expression of chromatin modifiers, including histone demethylases, broadly defined as lysine demethylases (KDMs), in lung macrophages. To investigate the role of KDMs in inflammation, we screened a panel of small-molecule inhibitors of chromatin modifiers for their efficacy in inducing anti-inflammatory macrophage polarization in vitro. We demonstrate that pretreatment with the broad-spectrum KDM inhibitor n-octyl-IOX1 and KDM5-specific inhibitor PB-IT resulted in a significant decrease of lipopolysaccharide (LPS)-induced expression of the inflammatory genes Il1b, Il6, Tnfa, and iNos in bone marrow-derived macrophages. Subsequent RNA sequencing and CUT&RUN analyses revealed that LPS activation led to distinct transcriptomic and epigenomic alterations, including expression of master transcription factors BLIMP-1 and GFI1, whereas n-octyl-IOX1 and PB-IT treatments rewired these regulatory networks, thereby impeding inflammatory gene expression. To further probe the merit of KDM inhibition in perturbing macrophage-mediated inflammation in vivo, we delivered n-octyl-IOX1 selectively to macrophages in mice using cell-specific, targeted lipidoid nanoparticles. n-octyl-IOX1 encapsulated nanoparticles significantly diminished LPS-mediated peritoneal macrophage expansion and inflammatory gene expression in this cell population, underscoring the importance of macrophage-specific targeting of KDMs with small-molecule inhibitors in inflammatory disease. - Source: PubMed
Publication date: 2026/07/06
Natarajan NiranjanaAhmed ThaybahGovindaswamy BalajiManickam Devika SDas JishnuIslam KabirulDutta Partha