Ask about this productRelated genes to: H1F0 antibody
- Gene:
- H1F0 NIH gene
- Name:
- H1 histone family member 0
- Previous symbol:
- H1FV
- Synonyms:
- H10
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-20
- Date modifiied:
- 2015-11-18
Related products to: H1F0 antibody
Related articles to: H1F0 antibody
- Pediatric gliomas, comprising both low-grade (LGGs) and high-grade gliomas (HGGs), exhibit significant molecular and clinical heterogeneity. While LGGs generally have a favorable prognosis, HGGs are associated with poor long-term survival despite aggressive treatment. Advances in molecular profiling have enabled targeted therapies, but treatment resistance and tumor heterogeneity remain major challenges. The integration of artificial intelligence (AI) and transcriptomic data holds promise for refining prognostic models and guiding personalized treatment strategies, yet its application in pediatric gliomas remains underexplored. - Source: PubMed
Publication date: 2026/03/09
Li GanglongPei FuyuWang Weizhen - Pulmonary fibrosis is a progressive disease that can lead to respiratory failure. Many types of cells are involved in the progression of pulmonary fibrosis. This study utilized quantitative proteomics to investigate the mechanism of TGF-β-induced fibrosis-like changes in mouse epithelial cells. Our findings revealed that TGF-β significantly impacted biological processes related to the endoplasmic reticulum, mitochondrion, and ribonucleoprotein complex. Pull-down assay coupled with proteomics identified 114 proteins that may directly interact with TGF-β, and their functions were related to mitochondria, translation, ubiquitin ligase conjugation, mRNA processing, and actin binding. Among them, 17 molecules were also found in different expression proteins (DEPs) of quantitative proteomic, such as H1F0, MED21, SDF2L1, DAD1, and TMX1. Additionally, TGF-β decreased the folded structure and the number of ribosomes in the endoplasmic reticulum and increased the expression of key proteins in the unfolded protein response, including HRD1, PERK, and ERN1. Overall, our study suggested that TGF-β induced fibrotic changes in mouse lung epithelial cells by ER stress and initiated the unfolded protein response through the PRKCSH/IRE1 and PERK/GADD34/CHOP signaling pathways. - Source: PubMed
Publication date: 2024/10/09
Li HengWang JinLi ZilingWu ZhidongZhang YanKong LingjiaYang QingqingWang DongShi HeShen GuozhengZou ShuangZhu WenqingFan KaiyuanXu Zhongwei - COVID-19 infections could be complicated by acute respiratory distress syndrome (ARDS), increasing mortality risk. We sought to assess the methylome of peripheral blood mononuclear cells in COVID-19 with ARDS. - Source: PubMed
Publication date: 2022/11/12
Bradic MartinaTaleb SarahThomas BinithaChidiac OmarRobay AmalHassan NessiyaMalek JoelAit Hssain AliAbi Khalil Charbel - Transcription dysregulation is a salient characteristic of bladder cancer (BC), but no appropriate therapeutic target for it has been established. Here, we found that heterogeneous downregulation of histone H4 transcription factor (HINFP) was associated with senescence in BC tissues and that lower HINFP expression could predict an unfavorable outcome in BC patients. Knockout of HINFP transcriptionally inhibited H1F0 and H1FX to trigger DNA damage, consequently inducing cell senescence to repress the proliferation and growth of BC cells. However, the senescence-associated secretory phenotype, characterized by increases in MMP1/3, enhances the invasion and metastasis of non-senescent BC cells. Histone deacetylase inhibitors (HDACis) could efficiently eliminate the senescent cells induced by HINFP knockout to suppress the invasion and metastasis of BC cells. Our study suggests that HDACis, widely used in multiple cancer types in a clinical context, may also benefit BC patients with metastases induced by cell senescence. - Source: PubMed
Publication date: 2022/06/06
Zheng XianchongLiu ZefuZhong JianliangZhou LiwenChen JiaweiZheng LisiLi ZhiyongZhang RuhuaPan JingxuanWu YuanzhongLiu ZhuoweiKang Tiebang - While germline variants in histone protein-encoding genes are emerging as the pathogenic mutations underlying rare, Mendelian disorders characterized by a conserved phenotype of neurodevelopmental syndrome coupled with craniofacial abnormalities, a systematic assessment of all human genes encoding histone proteins has not been performed to predict novel disease-candidate genes. We first defined a comprehensive list of 89 histone-encoding genes. We then analyzed which are most likely to underlay this conserved phenotype when mutated based on their intolerance to either missense or loss-of-function variation and based on their tissue expression profile. Strikingly few genes were found to be both ubiquitously expressed and significantly constrained against missense (7.9%, n = 7) or loss-of-function (6.7%, n = 6) variation. Notably, most of those significantly constrained genes encode replication-independent, variant histone proteins (7/7 in the missense analysis, 5/6 in the loss-of-function analysis). Of the seven genes predicted to be disease-causing when germline missense variation is present, three (H2AFV, H2AFY, H2AFY2) are novel disease-candidate genes. Five of the six genes predicted to be disease-causing with an underlying germline loss-of-function variant are novel disease-candidate genes (H2AFY2, H2AFZ, H2AFY, H2AFV, H1F0). These findings may serve as a focused reference for future sequencing of patients with the conserved phenotype. - Source: PubMed
Publication date: 2022/01/24
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