PAX9 antibody - N-terminal region (ARP34270_P050)
- Known as:
- PAX9 (anti-) - N-terminal region (ARP34270_P050)
- Catalog number:
- arp34270_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PAX9 antibody - N-terminal region (ARP34270_P050)
Related genes to: PAX9 antibody - N-terminal region (ARP34270_P050)
- Gene:
- PAX9 NIH gene
- Name:
- paired box 9
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-07
- Date modifiied:
- 2015-08-25
Related products to: PAX9 antibody - N-terminal region (ARP34270_P050)
Related articles to: PAX9 antibody - N-terminal region (ARP34270_P050)
- Tooth development or odontogenesis is a complex morphogenetic process that requires tightly regulated interactions between the oral epithelium and mesenchyme of neural crest origin. In this narrative review, we compile existing knowledge regarding gene regulatory networks and epigenetic factors throughout tooth development from initiation to eruption. Signaling between the epithelium and mesenchyme is mediated by four conserved pathways-Wnt/β-catenin, bone morphogenetic protein (BMP), fibroblast growth factor (FGF), and Sonic hedgehog (Shh)-which operate iteratively and interact through extensive crosstalk at each developmental stage. Transcription factors, such as PAX9, MSX1, PITX2, and LEF1, interpret these signals to control cell fate decisions and differentiation. Epigenetic modifications, including DNA methylation, histone modifications, and microRNA-mediated regulation, provide additional layers of control that fine-tune gene expression programs. Unlike existing reviews that address these regulatory mechanisms separately, here we integrate signaling pathways, transcription factor networks, epigenetic regulation, human genetic disorders, dental stem cell biology, and recent single-cell transcriptomic insights into a unified framework. We discuss opportunities to apply developmental biology knowledge towards regenerative dentistry goals, including iPSC-derived dental models and spatially resolved multi-omics approaches, while acknowledging the considerable gap between preclinical findings and clinical applications. - Source: PubMed
Publication date: 2026/03/30
Lee Dong-JoonWon Hyung-JinShin Jeong-Oh - Permanent maxillary canine agenesis is a rare condition caused by genetic, epigenetic, or environmental factors affecting tooth development. It results in malocclusion and adverse physiological changes. We present our orthodontic diagnosis, treatment challenges, and successful outcomes of a case involving a 10-year-old male with Class II/0 malocclusion, mild class III skeletal pattern, anterior crossbite, left mandibular lateral displacement malocclusion, right dental-skeletal crossbite, mild transitional bilateral posterior open bite, moderate lower anterior crowding, mild maxillary spacing, and genetic polymorphisms in MSX1 and PAX9; bilateral permanent maxillary canine agenesis, molar taurodontism, and bilateral mesioangular mandibular permanent second molar impactions. Presumptive mild-to-moderate hypolordosis and phase 2 left adolescent idiopathic scoliosis were also identified. Treatment involved widening the maxilla, replacing maxillary canines with bicuspids, second bicuspid extraction and closing spaces in the mandible, and deimpacting second mandibular molars. Spine follow-up showed indirect effects on head posture. Class I occlusion with normal overjet and overbite was achieved. Cervical spine correction occurred spontaneously years later. The spatiotemporal effects of MSX1 and PAX9 polymorphisms on the patient's phenotype led us to apply age-related orthodontic transverse and sagittal treatment strategies to avoid dental replacements and correct dental relationships and molar impactions. This approach also contributed to adolescent idiopathic scoliosis (AIS) self-correction in adolescence and long-term stability in adulthood. - Source: PubMed
Publication date: 2026/04/08
Gómez-Gil David FVásquez-Palacio GonzaloMarín-Botero Martha L - IntroductionCurrent cervical cancer screening guidelines recommend colposcopy referral for women co-positive for high-risk human papillomavirus (hrHPV) and abnormal cytology (≥ASC-US). However, cytology exhibits suboptimal sensitivity, and this strategy leads to high colposcopy burdens, especially in populations where non-HPV16/18 genotypes predominate. We evaluated a novel triage strategy using HPV16/18 genotyping and PAX1 methylation to optimize resource allocation.MethodsThis was a retrospective cohort study. In a cohort of 3,233 hrHPV-positive women who underwent HPV genotyping, liquid-based cytology (TCT), PAX1 methylation testing, colposcopy, and histopathological confirmation, we compared two strategies: (A) standard referral (hrHPV+ & TCT ≥ ASC-US); (B) novel referral (HPV16/18+ → immediate colposcopy; non-16/18 hrHPV+ → colposcopy if PAX1 methylation ΔCt ≤ 8.79). CIN3+ (CIN3 or cancer) served as the clinical endpoint.ResultsNon-16/18 hrHPV types (especially HPV52/58) accounted for over 30% of infections and 60% of CIN2+ lesions. PAX1 methylation was strongly associated with lesion severity (median ΔCt: chronic cervicitis 17.92 vs. CIN3 7.36 vs. cancer 5.97; < 0.001) and predicted CIN3+ with high accuracy (AUC = 0.82 in non-16/18 group). Strategy B detected 40 additional CIN3+ cases (+30.5%), reduced colposcopy referrals by 853 cases (absolute -25%, relative -46%), and increased the positive predictive value (PPV) from 6.6% to 14.6% (2.2-fold improvement) compared to Strategy A.ConclusionA triage algorithm combining HPV16/18 genotyping with PAX1 methylation significantly enhances CIN3+ detection while substantially reducing immediate colposcopies. This strategy is particularly well-suited for Chinese and other Asian populations where non-16/18 hrHPV types are prevalent, offering a more precise, cost-effective approach toward WHO's 2030 cervical cancer elimination goals. - Source: PubMed
Publication date: 2026/04/07
Fan XingGuo HaichunWang SifengPeng Xiangwen - There is a lack of cohesion in integrating current knowledge on the genetic and environmental etiology of dental impaction. The primary aim of this article is to review the current literature to identify candidate genes involved in the pathogenesis of dental impaction. A scoping review was conducted following PRISMA-ScR guidelines to identify and organize the available body of evidence. Relevant literature was searched in MEDLINE (via PubMed), Scopus, and Web of Science, with the final search conducted on 03 January 2026. Eligibility criteria included case-control, cohort, cross-sectional observational, and case report studies in humans. Selected studies focused on syndromic and non-syndromic variants, inheritance patterns, and genetic analyses. Risk of bias was assessed using the Joanna Briggs Institute (JBI) Critical Appraisal Checklists and AMSTAR 2. Only 18 studies met the eligibility criteria. Most articles were case reports and retrospective observational studies, revealing a multifaceted genetic landscape underlying dental impaction, with mutations affecting transcription factors and signaling pathways critical for odontogenesis, particularly , , , , and . Overall, the included studies showed moderate methodological quality. Current evidence does not clearly support specific genes as causal factors in dental impaction, but instead suggests a complex, likely polygenic susceptibility that modulates the anatomical threshold for tooth eruption. This review highlights , , , , and , as well as emerging candidates involved in eruption and bone remodeling pathways. Future progress depends on standardized phenotyping, large replicated cohorts, and functional studies linking genetic variation to dental follicle-mediated eruptive remodeling. - Source: PubMed
Publication date: 2026/02/26
Oliva-Ferrusola ElenaBaus-Domínguez MaríaTorres-Lagares DanielSerrera-Figallo Maria-Angeles - Cleft palate only (CPO) is a multifactorial craniofacial malformation with significant genetic and epigenetic contributions. Among these, microRNAs (miRNAs) have emerged as key regulators of palate development, although their alterations in CPO remain incompletely characterized. In this study, we performed a comprehensive miRNA expression analysis on palatal tissues from an Italian cohort of non-syndromic CPO patients, compared with a human embryonic palatal mesenchymal (HEPM) cell line. Using the NanoString nCounter platform for miRNA profiling, we identified significant deregulation of several miRNAs, notably the upregulation of miR-205-5p and miR-200c-3p and the downregulation of miR-125a-5p in CPO tissues. Based on these expression changes, a functional analysis was carried out to identify potential target genes. Validation in primary cell cultures derived from patient tissues confirmed these expression patterns. Functional analyses and target predictions implicated PAX9, a key transcription factor essential for palatogenesis, as a probable target of miR-205-5p, while miR-125a-5p was associated with the regulation of PRTG and PRSS35-genes involved in neural crest cell biology and extracellular matrix remodeling, respectively. Although modulation of certain predicted targets of miR-200c-3p was observed, in vitro inhibition experiments did not show significant changes in gene expression, highlighting the complexity of miRNA regulatory networks and the need for further studies to unravel these interactions. These findings identify miRNA alterations associated with CPO tissue and fibroblasts, highlighting novel candidate pathways for further mechanistic and therapeutic investigation. - Source: PubMed
Publication date: 2026/02/24
Palmieri AnnalisaScapoli LucaPellati AgneseApolloni FedericoZanchi ValerioSpinelli GiuseppeSgarzani RossellaCarinci FrancescoMartinelli Marcella