MSX1
- Known as:
- MSX1
- Catalog number:
- Y213371
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MSX1
Related genes to: MSX1
- Gene:
- MSX1 NIH gene
- Name:
- msh homeobox 1
- Previous symbol:
- HOX7
- Synonyms:
- HYD1, OFC5
- Chromosome:
- 4p16.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-26
- Date modifiied:
- 2019-04-23
Related products to: MSX1
Related articles to: MSX1
- 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 - Bovine tuberculosis (bTB) is a chronic, productivity-limiting infection in livestock with significant zoonotic potential that is caused by members of the Mycobacterium tuberculosis-complex (MTBC) which includes Mycobacterium bovis. Although the live, attenuated M. bovis bacillus Calmette-Guérin (BCG) vaccine licensed for use in people has been shown to protect cattle against bTB in experimental settings, its capacity to sensitize vaccinated animals to tuberculin used in bTB diagnosis is a major impediment to its use in livestock. As such, a bTB vaccine that will allow for the differentiation of M. bovis-infected animals among vaccinated animals (DIVA) is preferred. In a previous study, we reported that a recombinant Mycobacterium smegmatis strain engineered to express a functional MTBC type-7 ESX-1 secretion system called MSX-1 protects C57BL/6 mice against the causative agent of human TB, M. tuberculosis, without sensitizing the vaccinated mice to tuberculin. In this study, we wanted to determine if MSX-1 will also protect mice against M. bovis. Accordingly, we found that C57BL/6 mice vaccinated with MSX-1 and challenged with M. bovis had reduced burdens of bTB bacilli in their lungs and spleens and presented with reduced lung pathology. Furthermore, MSX-1 vaccination reduced bTB-mediated weight-loss and lethality in challenged mice. Consistent with previous observations, we found that mice vaccinated with MSX-1 did not become sensitized to tuberculin nor to a peptide fragment of EsxA, a potent T-cell antigen and secreted protein of the M. tuberculosis ESX-1 system. While the lack of sensitization in mice by MSX-1 to tuberculin and EsxA underscores its promise as a DIVA bTB vaccine, it suggests the mechanism of protection of MSX-1 may be CD4 and CD8 T-cell and IFN-γ independent and will require further investigation. Nevertheless, our results indicate MSX-1 is an effective bTB vaccine that deserves further development for use in livestock. - Source: PubMed
Publication date: 2026/04/02
Zriba SlimNiroula NirajanMcDonald SherinWhitecross DielleChen Jeffrey M - MSX1 variants are associated with autosomal dominant craniofacial developmental anomalies, including congenital tooth agenesis. Here, whole-exome sequencing in a Japanese patient with congenital tooth agenesis identified a novel de novo heterozygous frameshift variant in MSX1 (NM_002448.3:c.299delC). The variant is predicted to generate a truncated protein, p.(Pro100Argfs*60), that lacks the C-terminal region of MSX1 and is expected to result in loss of function. The patient presented with congenital tooth agenesis, including canine agenesis. Taken together with the genetic findings, this case supports the involvement of MSX1 in congenital tooth agenesis and broadens the reported phenotypic presentation of MSX1-related tooth agenesis. This report adds to the spectrum of disease-associated MSX1 variants and supports the utility of genomic testing for molecular diagnosis in rare dental developmental anomalies. - Source: PubMed
Publication date: 2026/04/02
Sano YasutoAndo MichiyoTokuyama-Toda ReikoOta AkikoMachida JunichiroSatomura KazuhitoGoto MitsuoTokita Yoshihito - 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