Ask about this productRelated genes to: FERD3L antibody
- Gene:
- FERD3L NIH gene
- Name:
- Fer3 like bHLH transcription factor
- Previous symbol:
- -
- Synonyms:
- NATO3, N-TWIST, bHLHa31
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-09
- Date modifiied:
- 2016-10-05
Related products to: FERD3L antibody
Related articles to: FERD3L antibody
- An in vivo approach combining high-throughput screening with cell type-specific readouts could enable elucidation of genotype-phenotype relationships in complex tissues. We developed an in vivo gain-of-function Perturb-seq platform, termed iGOF-Perturb-seq, to build a functional atlas of ~1000 transcription factors (TFs) in astrocytes, a cell type essential to many brain functions. We then identified cofunctional modules, annotated uncharacterized TFs, and predicted disease-associated TF clusters. Furthermore, iGOF-Perturb-seq performed in a mouse neuroinflammatory model identified as a therapeutic candidate, and astrocyte-specific overexpression of alleviated Alzheimer's disease symptoms in mice. This study provides resources for understanding gene regulation and disease mechanisms in vivo and for identifying potential therapeutic targets for different brain diseases. - Source: PubMed
Publication date: 2026/04/23
Zhang LianshengMa QiKong XiangruiZou WeijuanWang BoWu BinCai ShichengBai TaoTan RunlinDai ZijiLiu XingyuJia ZhihengZhang MeimeiLi TianwenZheng YuanyiHu XindeWu JianrongXu ZhengzhengZhou Haibo - Colorectal cancer (CRC) exhibits higher incidence and worse prognosis in males, yet the underlying molecular mechanisms remain incompletely understood. Epigenetic dysregulation, particularly histone modifications, plays a key role in CRC progression and metastasis. KDM5D, a Y-chromosome-encoded H3K4 demethylase, is frequently downregulated in male-predominant malignancies. Here, we explored the potential tumor-suppressive role of KDM5D and its downstream target FERD3L in male CRC. KDM5D and FERD3L expression were evaluated by immunohistochemistry in tumor and adjacent normal tissues from 60 male CRC patients, with correlations to clinicopathological features and survival analyzed. Functional effects of KDM5D overexpression were assessed in SW480 and HCT116 CRC cell lines using proliferation, colony formation, apoptosis, cell cycle, migration, and invasion assays. In vivo validation was performed in subcutaneous xenograft models. Mechanistic studies included ChIP-qPCR for promoter occupancy and H3K4me3 levels, along with rescue experiments using FERD3L overexpression. KDM5D expression was significantly reduced, while FERD3L was upregulated, in male CRC tumors compared with adjacent normal tissues, showing a strong inverse correlation (P < 0.001). Low KDM5D and high FERD3L levels were associated with advanced stage, lymph node metastasis, and poorer overall survival. KDM5D overexpression inhibited cell proliferation, colony formation, migration, and invasion while promoting apoptosis and G1 arrest in vitro. In vivo, KDM5D upregulation significantly suppressed subcutaneous tumor growth and promoted apoptosis, as confirmed by TUNEL assays. These effects were accompanied by reduced expression of mesenchymal markers (N-cadherin, vimentin) and increased E-cadherin. ChIP-qPCR revealed KDM5D recruitment to the FERD3L proximal promoter with concomitant reduction in H3K4me3 levels upon KDM5D overexpression. FERD3L overexpression partially rescued the suppressive phenotypes induced by KDM5D. KDM5D is recruited to the FERD3L promoter and associated with reduced H3K4me3 marks, correlating with transcriptional repression of FERD3L in male CRC. This axis is linked to the suppression of malignant progression and invasiveness in male CRC cells. These findings suggest a potential epigenetic mechanism contributing to sex-biased CRC behavior, warranting further validation in larger cohorts and functional studies of catalytic dependency. - Source: PubMed
Publication date: 2026/01/30
Yu JianweiZhong XuejingLan QinfenLan ShiqianLin ShuangmingQi YuanlinSu XuemeiDing Jian - The relationships of Paired Like Homeodomain 2 (PITX2), Ninjurin 2 (NINJ2), TWIST-Related Protein 1 (TWIST1), Ras Interacting Protein 1 (Rasip1), Solute Carrier Family 17 Member 3 (SLC17A3), Methylmalonyl Co-A Mutase (MUT) and Fer3 Like BHLH Transcription Factor (FERD3L) polymorphisms and gene expression with ischemic stroke have yet to be determined in Malaysia. Hence, this study aimed to explore the associations of single nucleotide polymorphisms (SNPs) and gene expression with ischemic stroke risk among population who resided at the Northern region of Malaysia. - Source: PubMed
Publication date: 2021/08/10
Ching Shu ChaiWen Lim JingIsmail Nor Ismaliza MohdLooi IreneKooi Cheah WeePeng Long SooMui Lee SoonTamibmaniam JayashamaniMuninathan PremaHooi Ong BengAli Siti Maisarah MdHassan Muhammad Radzi AbuMohamad Mohd SaberiGriffiths Lyn RWei Loo Keat - The floor plate of the developing midbrain gives rise to dopaminergic (DA) neurons, an important class of cells involved in Parkinson's disease (PD). Neural progenitors of the midbrain floor plate utilize key genes in transcriptional networks to drive dopamine neurogenesis. Identifying factors that promote dopaminergic neuron transcriptional networks can provide insight into strategies for therapies in PD. Using the chick embryo, we developed a quantitative PCR (qPCR) based method to assess the potential of a candidate factor to drive DA neuron gene expression, including the basic helix-loop-helix transcription factor Nato3 (Ferd3l). We then showed that overexpression of Nato3 in the developing chick mesencephalon produces a regionally dependent increase in genes associated with the DA neurogenesis, (such as Foxa2, Lmx1b and Shh) as well as DA neuron genes Nurr1 (an immature DA neuron marker) and mRNA expression of tyrosine hydroxylase (TH, a mature DA neuron marker). Interestingly, our data also showed that Nato3 is a potent regulator of Lmx1b by its broad induction of Lmx1b expression in neural progenitors of multiple regions of the CNS, including the midbrain and spinal cord. These data introduce a new, in vivo approach to identifying a gene that can drive DA transcriptional networks and provide the new insight that Nato3 can drive expression of key DA neuron genes, including Lmx1b, in neural progenitors. - Source: PubMed
Publication date: 2019/10/28
Peterson Doug JMarckini Darcy NStraight Jordan LKing Elizabeth MJohnson WilliamSarah Sarala SChowdhary Puneet KDeLano-Taylor Merritt K - Intracranial aneurysms (IA) are weakened outpouchings of the arterial wall in the cerebrovasculature. Rupture of an IA often leads to devastating consequences. The early identification of IA patients is crucial for management of their condition. A genetic variant at rs10230207, located nearby the HDAC9, TWIST1, and FERD3L genes, is associated with IA. HDAC9 is a class IIa histone deacetylase that mediates vascular smooth muscle cell dysfunction. TWIST1 is a mechanosensitive transcription factor and its expression is reduced in unstable carotid atherosclerotic plaques. In this study, the expression of the HDAC9, TWIST1, and FERD3L genes was characterized and associated with the presence of the rs10230207 genetic variant. Allelic discrimination and gene expression analysis were performed using lymphoblasts from 85 population controls and 109 IA patients. Subjects that were heterozygous (GT) within rs10230207 were 4.32 times more likely to have an IA than those that were homozygous for the reference allele (GG; 95%CI 1.23 to 14.16). Subjects that were homozygous (TT) were 8.27 times more likely to have an IA than those that were GG (95%CI 2.45 to 27.85). While the presence of the risk allele was not associated with changes in FERD3L gene expression, the risk allele was associated with increased HDAC9 and decrease in TWIST1 mRNA expression. The significant inverse correlation between HDAC9 and TWIST1 gene expression suggests that changes in the expression of both of genes may contribute to the formation of IAs. - Source: PubMed
Publication date: 2019/03/27
Lansdell Theresa AFisher CourtneySimmonds KentReeves Mat JWoo DanielDorrance Anne MDemel Stacie L