FoxH1 Peptide
- Known as:
- FoxH1 Peptide
- Catalog number:
- 3892BP-50
- Product Quantity:
- 50 ug
- Category:
- Peptides
- Supplier:
- Biovis
- Gene target:
- FoxH1 Peptide
Related genes to: FoxH1 Peptide
- Gene:
- FOXH1 NIH gene
- Name:
- forkhead box H1
- Previous symbol:
- -
- Synonyms:
- FAST1
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: FoxH1 Peptide
Related articles to: FoxH1 Peptide
- Formaldehyde is a colorless, strong-smelling chemical widely used in industrial and household products, including building materials and furniture manufacturing. Chronic exposure, even at low doses, has been associated with respiratory disease, neurotoxicity, immune dysregulation, and cancer. Although growing epidemiological evidence suggests a link between formaldehyde exposure and increased leukemia risk, the underlying molecular mechanisms remain poorly defined due to its high reactivity and limited biological traceability. In this study, we show that low-dose formaldehyde exposure (3 ppm) upregulates key oncogenic regulators-including RUNX1, ETV6, OCT4, and ISX-in B-ALL cell lines. Transcriptomic profiling combined with functional assays reveals that formaldehyde activates a RUNX1-ISX signaling axis, which in turn drives the expression of downstream oncogenic transcription factors (YBX2, HES2, FOXH1, MYCL, FOS, and PBX4). This activation reshapes transcriptional programs across major cancer-associated pathways, including metabolic signaling and hematopoietic cell-lineage regulation, ultimately promoting malignant activity and tumor formation in a xenograft model. Importantly, pharmacologic inhibition of the RUNX1-ISX axis significantly attenuated formaldehyde-induced oncogenic effects and reduced tumor growth. Analysis of human samples using immunofluorescence and Pearson correlation further confirmed a strong co-expression relationship between RUNX1 and ISX. Collectively, these findings identify the RUNX1-ISX axis as a critical mediator of formaldehyde-induced oncogenesis in B-ALL and highlight it as a promising therapeutic target for mitigating environmental leukemogenic risk. - Source: PubMed
Publication date: 2026/03/20
Lin Pei-ChinWang Li-TingYe Li-HengTseng Pin-YingHuang Pei-HsienHsu Wan-YiLiao Yu-MeiChiou Shyh-ShinHsu Shih-Hsien - Acute respiratory distress syndrome (ARDS) is a hypoxemic respiratory failure caused by severe pulmonary inflammation and progressive alveolar epithelial injury, and effective treatments are currently lacking. Our previous study demonstrated that the α-adrenergic receptor (α-AR) agonist phenylephrine (PE) alleviates lipopolysaccharide (LPS)-induced lung injury in ARDS mice by suppressing alveolar macrophage inflammation. However, whether alveolar epithelial cells (AECs)-critical components of the blood-air barrier for defense-contribute to PE's lung-protective effects remained unclear. - Source: PubMed
Publication date: 2026/03/23
Zeng ZhaojinYin YiyuanCong ZhukaiWei SenhaoWei XiaoyunShen ZiyuanGe QinggangZhu Xi - Polycomb Repressive Complex 2 (PRC2) establishes H3K27me3 marks to shape spatiotemporal gene expression during embryogenesis. While its dysregulation is linked to developmental disorders, cancer, and aging, the mechanisms guiding PRC2 to specific genomic loci remain a subject of ongoing debate. A prevailing model proposes that PRC2 recruitment occurs via its intrinsic affinity for chromatin rather than through sequence-specific transcription factors. Here, we provide evidence that the maternally deposited pioneer transcription factor Foxh1 plays a critical role in directing PRC2 to specific genomic loci during zygotic genome activation in . Foxh1 is a critical transcription factor mediating Nodal signaling, but it also plays an earlier role by pre-binding enhancers prior to signaling activation. This pre-binding is essential for forming enhanceosome complexes that trigger mesendodermal gene expression and drive gastrulation, in cooperation with other maternal transcription factors. Using maternal Foxh1-null embryos, we demonstrate that Foxh1 directly recruits Ezh2, the catalytic subunit of PRC2, to Foxh1-bound loci. Loss of Foxh1 impairs Ezh2 recruitment, leading to a global reduction in H3K27me3. These findings support a dual-function model in which Foxh1 not only activates endodermal gene expression in endoderm, but also recruits PRC2 to silence the same genes in ectoderm. This dual activity of Foxh1 allows the spatially coordinated epigenetic states of the endodermal gene regulatory program during early embryogenesis. - Source: PubMed
Publication date: 2025/09/22
Cho JinHendrickson Clark LMar NathanBlitz Ira LFish MargaretWang WenqiCho Ken W Y - For the first time, , whose pathogenic potential for humans has never been reported previously, has been identified to be associated with human infections. In this work, the phenotype of virulence, the potential genes that encode higher virulence of , and host responses to infection were investigated for the first time. It was found that S9 ( no. 9, isolated from the patient's bloodstream infection) was more virulent than both S8 ( no. 8, isolated from the patient's sputum) and S1 ( type strain ATCC13637). Candidate genes that may encode higher virulence of S9 were identified, including , , , and 14 other genes involved in porphyrin metabolism, pyrimidine metabolism, DNA methylation, two-component system, and biofilm formation. Transcriptome analysis of infected host cells (THP-1 cells) showed that 13 candidate genes involved in host response to hypoxia (, , , , , , , , , , , , and ) were preferentially upregulated by the more virulent strain S9 over the less virulent S8. Two downregulated genes ( and ) involved in monoatomic ion transport and the calcium signaling pathway may also need special attention, as they may be involved in pathogenesis. Antibiotic susceptibility testing indicated that strains S8 and S9 demonstrated high resistance to colistin and polymyxin B, with MIC values surpassing clinical breakpoints. For ceftazidime (a cephalosporin) and levofloxacin (a fluoroquinolone), MIC values were elevated in S8/S9 compared to S1 but remained within the susceptible range (ceftazidime: S8 and S9; levofloxacin: S8) or intermediate category (levofloxacin: S9). Because of the above differences in virulence properties and antibiotic susceptibility, it is critical that be distinguished from in a clinical setting for improved care. This work provides the basis for future studies on pathogenic mechanisms of and for developing improved treatment in the future. - Source: PubMed
Publication date: 2025/09/23
Liu JiayingDong XuXiang YanghuiLi YiYu YuyunWu TiantianYuan XinCao DanZhang HanyinZhu LixiaZhang Ying - Porcine extended potential stem cells (pEPSCs), which exhibit both self-renewal and pluripotency, are promising for application in both agricultural biotechnology and regenerative medicine. However, the molecular mechanisms governing these two interconnected properties remain elusive. Here, two types of CRISPR-Cas9 screenings are conducted in pEPSCs. This fitness screening identified several genes essential for cell viability, including PRMT1, MYBL2, and NASP. Concurrently, FACS-based screenings revealed genes crucial for pluripotency, such as SOX2, ZFP42, and FOXH1. Notably, it is demonstrated that FOXH1 is required for maintaining pluripotency in pEPSCs, which complements the understanding of its role in mesendoderm specification. pEPSCs lacking FOXH1 exhibited a flatter and more dispersed clonal morphology, accompanied by downregulation of pluripotency genes and upregulation of lineage-specific genes. Additionally, FOXH1 knockdown significantly impaired blastocyst formation during early pig embryogenesis. Functionally, the dual role of FOXH1 in pluripotency maintenance and cell differentiation is validated: FOXH1 preserves pluripotency by enhancing chromatin accessibility at pluripotency gene loci, while also influencing lineage specification through H3K4me3 modification at developmental related genes. Thus, these findings uncover a novel role of FOXH1 involved in the core regulatory network that orchestrates gene expression programs to maintain the pluripotency state of pEPSCs and provide valuable insights into categorizing gene function. - Source: PubMed
Publication date: 2025/07/11
Su PengWu LinhuiLi DelongSong WentingTao DagangLiu LiangWang QiGao ManxinXu TianLiu XinXie ShengsongZhang XiaZhou JilongMiao Yi-Liang