HOXA2 antibody - middle region (ARP31950_P050)
- Known as:
- HOXA2 (anti-) - middle region (ARP31950_P050)
- Catalog number:
- arp31950_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HOXA2 antibody - middle region (ARP31950_P050)
Related genes to: HOXA2 antibody - middle region (ARP31950_P050)
- Gene:
- HOXA2 NIH gene
- Name:
- homeobox A2
- Previous symbol:
- HOX1K
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-18
- Date modifiied:
- 2015-08-25
Related products to: HOXA2 antibody - middle region (ARP31950_P050)
Related articles to: HOXA2 antibody - middle region (ARP31950_P050)
- Little is known about how three-dimensional chromatin topology shapes mammalian craniofacial development. In mouse cranial neural crest cells, a Polycomb Repressive Complex 2 (PRC2)-dependent chromatin architecture is established before migration. This configuration maintains craniofacial gene promoters poised and connects them with distal Polycomb tethering elements, positioning promoters in spatial proximity to future long-range enhancers. Deletion of Ezh2 disrupts this early topology, causing inappropriate gene derepression in post-migratory craniofacial subpopulations where these genes are normally silenced, and failure of long-range enhancer recruitment where activation is required, thereby impairing proper gene expression. We further identify a distal Polycomb tethering element essential for Hoxa2 enhancer recruitment across topologically associating domains. Thus, Polycomb acts not only as a transcriptional repressor, but also as a chromatin-folding organizer that prepares developmental genes for later activation, by facilitating subsequent recruitment of distal active enhancers previously not in contact. Polycomb-mediated topology therefore orchestrates the transition from progenitor plasticity to precise spatiotemporal control of morphogenetic gene programs during neural crest development and face formation. - Source: PubMed
Publication date: 2026/05/14
Ben Zouari YousraJoshi OnkarSalvi AdwaitKessler SandraDucret SebastienRoss FionaHolwerda Sjoerd J BVilain NathalieMamilla-Sanivaram SoujanyaSmallwood SebastienKohler HubertusStadler Michael BMinoux MarylineRijli Filippo M - Site-directed mutagenesis of TaHOX2 homoeologs enhances floret fertility and grain number in wheat. - Source: PubMed
Publication date: 2026/04/26
Li MingjiuZhang HaiyanGao GuofengJiao Yuling - The gene, a recently identified regulator of embryonic development and stem cell pluripotency, is essential for embryonic survival, as its homozygous knockout () leads to lethality in mice at approximately embryonic day 12.5 (E12.5). To elucidate the underlying lethal mechanism, an integrated approach combining morphological observation, multi-stage transcriptomic analysis, and functional validation experiments was employed to systematically investigate the developmental disorders caused by deficiency. Morphological observation showed that / embryos exhibited significant abnormalities at developmental stages E9.0, E9.5, E10.0, E10.5, and E11.0, including shortened body axis, defective neural tube closure, aberrant somite differentiation, and cardiovascular malformations, accompanied by overall developmental delay. At the molecular level, through RNA sequencing and qRT-PCR validation revealed that deficiency not only suppressed the expression of genes critical for somitogenesis (, ), neurodevelopment (, ), and the hematopoietic system (, ), but also aberrantly activated genes associated with apoptosis (, ) and lipid metabolism (, ). TUNEL staining showed that the level of apoptosis was significantly increased in embryos. Meanwhile, immunofluorescence detection of Hif-1α indicated that the hypoxic stress response was aberrantly activated. Furthermore, the widespread dysregulation of genes involved in thyroid hormone transport (), DNA damage stress (), and lipid metabolism (, ) collectively exacerbated the developmental imbalance, ultimately leading to embryonic death. A cross-species analysis demonstrated that knockdown in human embryonic stem cells (hESCs) significantly suppressed the expression of core angiogenic genes (, and ), a finding consistent with public database analyses indicating a strong association between and the hypoxic response. In conclusion, this study elucidates that functions as a regulatory gene that maintains embryonic homeostasis by orchestrating multiple key developmental processes, including somitogenesis, neural differentiation, angiogenesis, and the hypoxic stress response. This discovery not only deepens the understanding of the role of in embryonic development but also provides a new perspective for deciphering the pathogenesis of related hereditary diseases. - Source: PubMed
Deng Ya-XinDing Bao-JunLi Hong-ChunChen SongZhang YingZhou BoZhang Zhen - Craniofacial microsomia (CFM), a congenital anomaly stemming from first and second branchial arch dysplasia, poses challenges due to its diverse clinical manifestations, necessitating a comprehensive understanding of its complex etiology. We explored gene-environment interactions in CFM, focusing on genetic factors, and environmental influences, aiming to enhance insights into its multifactorial origins and guide future research. Genetic studies suggest HOXA2, PAX3, and TBX1 as potential susceptibility genes, while epidemiological research links maternal smoking, diabetes, and alcohol use to increased risk. Gene-environment interactions may impact craniofacial development via epigenetic mechanisms, though the exact pathways remain unclear. Future studies should expand CFM cohorts for better G×E risk assessment and apply multiomics approaches to clarify mechanisms. Functional validation via animal models and stem cells will verify genetic and environmental impacts. Advancing personalized medicine with early screening, precise diagnostics, and prevention remains crucial for high-risk cases. - Source: PubMed
Publication date: 2026/03/10
Li ZhifengQi WeikunZang TianyinLiu WeiZhang Zhiyong - Relieving renal fibrosis are promising therapeutic strategies for chronic kidney disease (CKD). Here we showed that decreased homeobox A2 (HOXA2) expression with excessive ER stress activation were observed in the renal tissues of UUO mice established on male C57BL/6 mice and TGF-β1-induced human proximal tubular epithelial cells (HK-2 cells). After transfected HOXA2 overexpression plasmids into HK-2 cells and administered adeno-associated virus (AAV) containing HOXA2 to UUO mice, the expression of ER stress markers such as ATF6, GRP78 and CHOP decreased, renal dysfunction and fibrosis were significantly attenuated. Mechanistically, HOXA2 binds to the SIRT1 promoter, enhancing SIRT1 transcription and deacetylase activity, which led to ATF6 deacetylation and downregulation. The protective effect of HOXA2 was confirmed against the ER stress agonist thapsigargin. Moreover, DNMT1-mediated promoter methylation was identified as a potential mechanism for HOXA2 suppression in fibrosis. Targeting HOXA2 maybe an innovative therapeutic strategy for fibrosis treatment in CKD. - Source: PubMed
Publication date: 2025/12/30
Li XinMa Tian-KuiDeng Xiao-XuHai SangMa FangZou YunYang QiLyu HuiLi Yu-XiDing Hong