HOXA2 Reverse PCR Primer (300bp position)
- Known as:
- HOXA2 Reverse PCR test kit Primer (300bp position)
- Catalog number:
- MP1150
- Product Quantity:
- ea
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- HOXA2 Reverse PCR Primer (300bp position)
Related genes to: HOXA2 Reverse PCR Primer (300bp position)
- 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 Reverse PCR Primer (300bp position)
Related articles to: HOXA2 Reverse PCR Primer (300bp position)
- Bone repair is a complex repair process involving various factors. Carbon dioxide (CO) therapy has been shown to accelerate fracture repair and bone healing. The present study aimed to explore the effects of CO-releasing hydrogels on osteoblast formation and the involvement of interferon regulatory factor-1 (IRF1) and homeobox A2 (HOXA2) during this process. The effects of CO-releasing hydrogels on MC3T3-E1 cells were evaluated using a CCK-8 assay for cell proliferation, Western blotting for protein expression, and alizarin red S staining for osteogenic capacity. The relationship between IRF1 and HOXA2 was assessed by bioinformatics analysis, dual-luciferase reporter assays, and chromatin immunoprecipitation assays. Co-transfection experiments were conducted to investigate the impact of HOXA2 overexpression on osteoblast formation under IRF1 knockdown conditions. A mouse bone defect model was established to validate the effects of CO-releasing hydrogels and the involvement of IRF1 and HOXA2 in vivo. CO-releasing hydrogels positively regulated MC3T3-E1 cell proliferation, bone formation-related protein expression, ALP activity, and osteogenic capacity. IRF1 was significantly upregulated in hydrogel-treated cells and demonstrated a pivotal role in osteoblastogenesis. IRF1 targeted and regulated the expression of HOXA2. Importantly, overexpression of HOXA2 mitigated the effects of IRF1 knockdown on osteoblast formation. In the in vivo mouse model, CO-releasing hydrogels accelerated bone healing by promoting collagen deposition, bone mineralization, and upregulating bone formation-related factors. This study highlights the significant potential of CO-releasing hydrogels and unveiled the regulatory effects of IRF1 and HOXA2 in promoting osteoblast differentiation and bone healing. These findings may facilitate the development of therapeutic strategies aimed at enhancing bone regeneration and promoting effective healing. - Source: PubMed
Publication date: 2026/08/12
Dai ShiyouFeng LiFan XiaoLao KechengDing BoxiaLiu Yanqun - - Source: PubMed
Publication date: 2026/07/31
Bechara AhmadLaumonnerie ChristopheVilain NathalieKratochwil Claudius FCankovic VanjaMaiorano Nicola AKirschmann Moritz ADucret SebastienRijli Filippo M - The synergistic crosstalk between epigenetic dysregulation and metabolic reprogramming underlies to prostate cancer (PCa) development and treatment resistance, yet an integrated prognostic signature reflecting this nexus remains poorly defined. We developed and validated a gene signature associated with methylation and amino acid metabolism for patient stratification and exploring its connection to tumor microenvironment (TME) remodeling. RNA sequencing data and independent datasets were integrated with predefined gene sets for DNA methylation (n = 79) and amino acid metabolism (n = 471). A analytical workflow was employed: identification of hub genes and least absolute shrinkage and selection operator (LASSO)-Cox modeling; construction of a prognostic nomogram; comprehensive TME profiling; and validation through single-cell RNA sequencing (scRNA-seq) cellular dynamics analysis and immunohistochemistry (IHC) on a prostate cancer tissue microarray. A novel six-gene prognostic model (ASPM, WDR86, CCK, HOXA2, EGF, ZFHX4) was developed. This model efficiently discriminates patients into groups based on risk level though divergent overall survival (p < 0.001) and exhibited high predictive accuracy in external validation sets (3-year area under the curve (AUC) = 0.87). A nomogram incorporating the signature, pathologic T stage, and Gleason score surpassed individual clinical factors (5-year AUC = 0.73). Functional annotation indicated that high-risk tumors were characterized by downregulated androgen response and activated E2F/G2M checkpoint pathways. The signature was correlated with an immunosuppressive TME, which was supported by a negative correlation between ZFHX4 and monocyte infiltration (r = -0.37, p < 0.001) and a positive correlation between ASPM and activated CD4T cells (r = 0.44, p < 0.001). Single-cell trajectory analysis exhibited that epithelial cells, fibroblasts, and natural killer T (NKT) cells was key cellular expressors of the signature. We utilized immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (qRT-PCR) to confirm the differential expression. We developed and validated an integrative methylation-amino acid metabolism gene signature that effectively predicts prognosis and reflects an immunosuppressive TME in PCa. This study provides a translational framework for precision oncology, bridging epigenetic-metabolic crosstalk to disease aggressiveness, and offers potential biomarkers for informing risk-stratified therapy and immunotherapy approaches. - Source: PubMed
Zhang ChaoLiu LikunWu Kai - 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