Ask about this productRelated genes to: HOXB5 antibody
- Gene:
- HOXB5 NIH gene
- Name:
- homeobox B5
- Previous symbol:
- HOX2, HOX2A
- Synonyms:
- -
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-09-07
Related products to: HOXB5 antibody
Related articles to: HOXB5 antibody
- HOX genes encode transcription factors that are central regulators of cell fate during embryogenesis and of maintaining respective positional cell identity throughout life. Moreover, HOX factors shape the specification of regional properties of the respective tissues, but detailed information regarding the role of HOX genes in the adult human respiratory system is still lacking. - Source: PubMed
Publication date: 2026/07/14
Budeus BettinaKlein Diana - Histone lactylation, a novel posttranslational modification driven by glycolytic lactate, has emerged as a key regulator of tumorigenesis. However, its role in osteosarcoma (OS) progression and the underlying metabolic‒epigenetic crosstalk remain poorly understood. - Source: PubMed
Publication date: 2026/06/26
Wang HaoWu ZhongxuanYang RuiXu ShenglinYao ShunjieWu ZihengXiao LongzeQue YukangHe PengMa QimingXu TangbingWei WeiHu Yong - Irisquinone is an active bioactive constituent isolated from the dried rhizomes of Iris tectorum, a traditional Chinese medicinal herb. Accumulating evidence has confirmed that irisquinone exhibits prominent antitumor activity against a variety of human malignancies. Nevertheless, its biological function and precise molecular mechanisms underlying anti-osteosarcoma effects remain poorly clarified. In the present study, we systematically explored the inhibitory effect of irisquinone on osteosarcoma progression via a combination of in vitro cell experiments and in vivo xenograft model validation. Network pharmacology and molecular docking were applied as preliminary computational strategies to predict potential therapeutic targets and downstream signaling pathways of irisquinone. Bioinformatics analysis indicated that the PI3K/AKT signaling axis is closely implicated in the anti-osteosarcoma action of irisquinone, with AKT1 predicted as a core potential target. Further in vitro functional experiments verified that irisquinone markedly suppressed the proliferation and migration capacity of osteosarcoma cells. Mechanistically, irisquinone restrained the activation of the PI3K/AKT signaling pathway, modulated the expression of apoptosis-related Bcl-2 family proteins (Bax and Bcl-2), and ultimately triggered osteosarcoma cell apoptosis. In addition, the anti-tumor effect and pathway regulatory activity of irisquinone were further validated in vivo. Collectively, our findings demonstrate that irisquinone exerts its anti-osteosarcoma function, at least in part, through suppressing the PI3K/AKT signaling pathway. This work provides reliable experimental support and a theoretical foundation for the preclinical application of irisquinone and the development of novel therapeutic agents against osteosarcoma. - Source: PubMed
Publication date: 2026/06/10
Wu ZihengLi XingxingYao ShunjieWang HaoWang YuDing YanchaoHu Yong - hox genes are evolutionarily conserved transcription factors essential for anterior-posterior body patterning, yet their specific contributions to cardiac morphogenesis and calcium signaling remain elusive. Using zebrafish as a model for vertebrate cardiogenesis, we dissected the distinct roles of hoxb5a and hoxb5b-two paralogues retained after the teleost-specific genome duplication. CRISPR/Cas9-mediated knockout of hoxb5a or hoxb5b revealed divergent functions: loss of hoxb5a caused pericardial edema, abnormal cardiac looping, and defective ventricular morphology, whereas hoxb5b mutants developed normally and survived to adulthood. Comprehensive functional analyses combining high-speed videography, calcium optical imaging, and electrocardiography demonstrated that hoxb5a deficiency leads to impaired contractility and conduction, associated with disrupted calcium transients. Transcriptomic profiling further revealed that hoxb5a and hoxb5b exert antagonistic regulation of genes controlling excitation-contraction coupling and calcium handling in cardiomyocytes. These findings demonstrate a functional divergence between hoxb5a and hoxb5b in the genetic regulation of teleost cardiac development. hoxb5a plays a dominant role in coordinating early cardiac morphogenesis and calcium homeostasis, whereas hoxb5b acts as an auxiliary regulator. This antagonistic interaction highlights how gene duplication and divergence refine the transcriptional networks that govern cardiac patterning. Our study uncovers an unrecognized link between hox gene activity and calcium-dependent signaling, providing new mechanistic insights into the evolutionary control of heart development and potential pathways contributing to congenital heart disease. - Source: PubMed
Publication date: 2026/04/15
Zu YaoJia HaiwangWang BingqiXu HaoHe HongyangChen Liangbiao - Hao-Fountain syndrome (HAFOUS) is a rare autosomal dominant neurodevelopmental disorder caused by pathogenic variants. A diagnostic blood DNA methylation episignature has been established, yet the broader regulatory consequences of haploinsufficiency and their tissue specificity remain incompletely characterized. - Source: PubMed
Publication date: 2026/02/20
van der Laan LiselotZwart RobVenema AndreaMul Adri NHaagmans Martin AHulsbosch BartDyment DavidValenzuela IreneCaro PilarSailer SebastianSchaaf Christian PSadikovic BekimMannens Marcel M A Mvan Haelst Mieke MPurushothama Manasa KalyaHenneman Peter