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 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 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 regulatory over 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 the 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 insight 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 - - Source: PubMed
Publication date: 2026/02/16
Quinn Callum JVelasco Epiphany SWehrens Xander H T - The current study investigated the proangiogenic effects of fraction VII of perivitelline fluid (hscPVF-VEGF) obtained from the late-stage embryos of Indian horseshoe crab (Tachypleus gigas; Müller) using human umbilical cord tissue-derived MSCs (hUCMSCs). Angiogenic potential of hscPVF-VEGF was investigated by analyzing transcripts of signature angiogenic markers, key transcription factors and matrix metalloproteases. Molecular docking studies were performed to predict the binding site of hscPVF-VEGF with the VEGF receptor (VEGFR). hscPVF-VEGF significantly upregulated VEGF, vWF, and downregulated sFlt-1. Significant increase in transcriptional levels of HOXA7, HOXB3, HOXB5, CD31, MMP2, and MMP9 further elucidated the molecular mechanism underlying the angiogenic ability of hscPVF-VEGF. Wound healing assay revealed the migratory potential of hscPVF-VEGF. Molecular docking studies predicted that hscPVF-VEGF may modulate hVEGFR activity by binding in a pocket within the extracellular domains (D5, D6, and D7) distal to the VEGF binding site (D2 and D3). This study infers the potential and molecular mechanism of hscPVF-VEGF inducing angiogenic differentiation in hUCMSCs, suggesting clinical application of a recombinant form of hsPVF-VEGF in disorders with dysfunctional angiogenesis. - Source: PubMed
Publication date: 2026/01/16
Aghila Rani K GPandit HrishikeshSubedi RambhadurOtiv-Pandit SayliJogdand Anil BankatiGupta HajraFandilolu PrayagrajRokade SushamaIdicula-Thomas SusanChatterji AnilMadan Taruna - HOXB5, a member of the homeobox (HOX) gene family. Its dysregulated expression has been increasingly reported across multiple human cancers, where it correlates with malignant progression and poor clinical outcomes. A concise synthesis of its regulatory networks and cancer-associated functions is therefore needed to clarify its biological and translational significance. - Source: PubMed
Publication date: 2026/01/06
Zhong KuiYi QiangChen ZhengXu YongchangZeng YangnengZhong Jinghua