GO:0070172 positive regulation of tooth mineralization: Regulatory Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0070172 (positive regulation of tooth mineralization) is a biological process that increases the deposition of calcium salts in tooth structures, as defined by QuickGO.
• Key molecular drivers include the neurotrophin receptor p75NTR (NGFR), the transcription factor Trps1, the circadian regulators BMAL1/CLOCK, and microRNA-21 [1,2,4,7].
• p75NTR promotes tooth rhythmic mineralization by upregulating BMAL1/CLOCK, linking circadian rhythm to incremental growth lines in teeth [1,7].
• Trps1 regulates mineralization of dental tissues and proliferation of tooth organ cells, with mutations linked to tricho-rhino-phalangeal syndrome.
• Amelogenin gene expression is developmentally regulated during tooth development and serves as a marker of enamel mineralization.
• Emerging evidence implicates KDM6B/Pdk1 glycolytic pathway-driven ZEB2 lactylation in cellular cementum formation, and Ctsk+ osteoclasts in condylar morphogenesis via hypoxic lysosome [6,8].
Description
Tooth mineralization is the biological process by which calcium salts are deposited into the organic matrix of enamel, dentin, and cementum, giving teeth their hardness and structural integrity. The Gene Ontology term GO:0070172, positive regulation of tooth mineralization, describes any process that activates or increases the frequency, rate, or extent of this deposition [1,2]. This term is critical for researchers studying craniofacial development, dental tissue engineering, and pathologies such as amelogenesis imperfecta, dentinogenesis imperfecta, and ectopic calcification. Understanding its positive regulators helps explain how teeth achieve their precise architecture and how disruptions lead to mineralization disorders [4,5]. Recent studies have identified diverse molecular players in this process, including the neurotrophin receptor p75NTR, which promotes tooth rhythmic mineralization via upregulation of BMAL1/CLOCK, and the transcription factor Trps1, which regulates mineralization of dental tissues. The spatiotemporal expression of p75NTR during early tooth development further underscores its role in mineralization regulation. Additionally, microRNA-21 has been shown to facilitate osteoblast activity, indirectly supporting mineralized tissue formation. These findings highlight the complexity of positive regulation of tooth mineralization and its relevance to both developmental biology and clinical dentistry.
positive regulation of tooth mineralization At A Glance
| GO ID | GO:0070172 |
|---|---|
| GO term | positive regulation of tooth mineralization |
| Ontology | biological_process |
| Synonym | none |
| Major function | Activates or increases the deposition of calcium salts in tooth structures |
| Related process | Tooth mineralization (GO:0034505) |
| Key regulators | p75NTR (NGFR), Trps1, BMAL1/CLOCK, microRNA-21, KDM6B, ZEB2, Ctsk |
| Associated diseases | Tricho-rhino-phalangeal syndrome, dental mineralization disorders, ectopic calcification |
| Research methods | CRISPR knockout, knock-in, overexpression, RNA-seq, imaging, histological staining |
What Is GO:0070172?
GO:0070172, positive regulation of tooth mineralization, is defined by QuickGO as any process that activates or increases the frequency, rate or extent of tooth mineralization, the deposition of calcium salts in tooth structures. In simpler terms, it encompasses all molecular and cellular events that boost the formation of mineralized dental tissues, including enamel, dentin, and cementum. This biological process is essential for proper tooth development and maintenance, and its dysregulation can lead to dental defects or pathological calcification [1,2,4].
Why Is positive regulation of tooth mineralization Important in Cell Biology?
Positive regulation of tooth mineralization is fundamental to dental health and craniofacial development. It ensures that teeth acquire the necessary hardness and durability to withstand mechanical forces during mastication. Disruptions in this process can result in hypomineralized teeth, increased susceptibility to caries, and structural abnormalities. Moreover, understanding the positive regulators of mineralization provides insights into regenerative dentistry and the development of biomaterials for dental repair [1,4,5]. The identification of p75NTR as a promoter of rhythmic mineralization via BMAL1/CLOCK highlights a link between circadian biology and dental tissue formation, opening new avenues for research [1,7]. Similarly, the role of Trps1 in dental mineralization connects this process to a broader spectrum of developmental syndromes. As such, GO:0070172 is a focal point for both basic and translational dental research.
• Essential for proper enamel, dentin, and cementum formation, ensuring tooth hardness and function [1,2].
• Dysregulation leads to dental mineralization disorders such as amelogenesis imperfecta and dentinogenesis imperfecta [4,5].
• p75NTR-mediated regulation links circadian rhythm to tooth incremental growth lines, impacting developmental timing [1,7].
• Trps1 mutations cause tricho-rhino-phalangeal syndrome, which includes dental abnormalities.
• MicroRNA-21 facilitates osteoblast activity, indirectly promoting mineralized tissue formation.
• KDM6B/Pdk1 glycolytic pathway and ZEB2 lactylation drive cellular cementum formation, a key component of tooth root attachment.
• Ctsk+ osteoclasts orchestrate condylar morphogenesis via hypoxic lysosome, affecting temporomandibular joint development.
• Amelogenin gene expression is a marker of enamel mineralization and is developmentally regulated.
• Understanding positive regulation aids in developing strategies for dental tissue engineering and regeneration [1,4].
• Provides a model for studying biomineralization processes in other tissues, such as bone [3,6].
What Happens During positive regulation of tooth mineralization?
Initiation of Mineralization: Role of p75NTR and Circadian Regulators
In simple terms: Certain proteins act like switches that turn on the mineralization process, and some of these switches are controlled by the body's internal clock.
The neurotrophin receptor p75NTR (encoded by NGFR) is a key positive regulator of tooth mineralization. It promotes tooth rhythmic mineralization by upregulating the circadian clock genes BMAL1 and CLOCK. The spatiotemporal expression of p75NTR during early tooth development suggests it plays a role in initiating mineralization events. Furthermore, p75NTR has been implicated in the regulation of circadian rhythm and incremental growth lines during tooth development, indicating that it couples the circadian clock to the daily deposition of mineralized tissue. This regulation ensures that mineralization occurs in a rhythmic pattern, contributing to the characteristic incremental lines seen in teeth.
Transcriptional Control: Trps1 and Amelogenin
In simple terms: Special transcription factors control which genes are turned on to build the tooth's mineralized matrix.
The transcription factor Trps1 regulates the mineralization of dental tissues and the proliferation of tooth organ cells. Mutations in Trps1 lead to tricho-rhino-phalangeal syndrome, which includes dental abnormalities, highlighting its importance in positive regulation of tooth mineralization. Another critical gene is amelogenin (AMELX), whose expression is tightly regulated during tooth development and serves as a marker for enamel mineralization. The regulation of amelogenin gene expression is essential for proper enamel formation, and its dysregulation can lead to amelogenesis imperfecta.
Osteoblast and Cementum Formation: MicroRNA-21 and KDM6B/ZEB2 Pathway
In simple terms: Cells that build bone-like tissues in teeth are activated by specific microRNAs and metabolic pathways.
MicroRNA-21 facilitates osteoblast activity, which indirectly supports tooth mineralization by promoting the formation of mineralized matrix. In the context of cementum, a recent study identified that the KDM6B/Pdk1 glycolytic pathway-driven ZEB2 lactylation promotes cellular cementum formation. This pathway involves epigenetic regulation and metabolic reprogramming, leading to increased cementum deposition. These findings expand the understanding of positive regulation of tooth mineralization beyond enamel and dentin to include cementum, which is crucial for tooth root attachment.
Osteoclast Regulation and Condylar Morphogenesis: Ctsk+ Osteoclasts
In simple terms: Bone-resorbing cells also play a role in shaping the jaw joint and influencing mineralization.
Ctsk-positive osteoclasts orchestrate condylar morphogenesis via hypoxic lysosome. Although osteoclasts are typically associated with bone resorption, their activity is tightly coupled with bone formation and mineralization. In the condyle, which is part of the temporomandibular joint, osteoclasts contribute to shaping the mandibular condyle and indirectly influence mineralization. This highlights the intricate balance between resorption and formation in positive regulation of tooth mineralization.
Integration of Signaling Pathways
In simple terms: Multiple signals work together to ensure teeth mineralize correctly.
The positive regulation of tooth mineralization integrates various signaling pathways, including neurotrophin signaling via p75NTR [1,2,7], transcriptional regulation by Trps1, microRNA-mediated osteoblast activation, and metabolic-epigenetic crosstalk involving KDM6B, Pdk1, and ZEB2. These pathways converge to control the expression of mineralization-related genes such as amelogenin and to coordinate the activity of odontoblasts, ameloblasts, cementoblasts, and osteoblasts. Disruption of any of these components can lead to mineralization defects, underscoring the complexity of this biological process.
Key Genes Involved in GO:0070172 positive regulation of tooth mineralization
The following genes and proteins have been experimentally implicated in the positive regulation of tooth mineralization, based on the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| NGFR (p75NTR) | Promotes tooth rhythmic mineralization via upregulation of BMAL1/CLOCK; regulates circadian rhythm and incremental growth lines | Key regulator linking circadian clock to mineralization; potential target for modulating mineralization timing [1,2,7] |
| BMAL1 (ARNTL) | Core circadian clock transcription factor; upregulated by p75NTR to promote rhythmic mineralization | Mediates circadian control of mineralization; knockout models show disrupted incremental lines [1,7] |
| CLOCK | Core circadian clock transcription factor; partners with BMAL1 | Essential for circadian regulation of mineralization; targets for rhythm studies |
| TRPS1 | Transcription factor regulating mineralization of dental tissues and proliferation of tooth organ cells | Mutations cause tricho-rhino-phalangeal syndrome with dental abnormalities; model for transcriptional control |
| AMELX | Amelogenin; major enamel matrix protein; marker of enamel mineralization | Developmental regulation studied; mutations cause amelogenesis imperfecta |
| MIR21 (microRNA-21) | Facilitates osteoblast activity | Indirectly promotes mineralized tissue formation; potential therapeutic target |
| KDM6B | Histone demethylase; part of KDM6B/Pdk1 glycolytic pathway | Drives cellular cementum formation via ZEB2 lactylation; epigenetic regulator |
| PDK1 | Pyruvate dehydrogenase kinase 1; glycolytic pathway component | Involved in metabolic reprogramming for cementum formation |
| ZEB2 | Transcription factor; target of lactylation | Lactylation promotes cellular cementum formation; links metabolism to transcription |
| CTSK | Cathepsin K; marker of osteoclasts | Ctsk+ osteoclasts orchestrate condylar morphogenesis via hypoxic lysosome |
| RUNX2 | Master transcription factor for osteoblast differentiation | Indirectly supports mineralization; not directly cited in provided list but commonly studied |
| SP7 (Osterix) | Transcription factor essential for osteoblast differentiation | Indirectly supports mineralization; not directly cited in provided list |
| BGLAP (Osteocalcin) | Late marker of osteoblast differentiation and mineralization | Used as a marker for mineralized tissue formation; not directly cited |
| ALPL | Alkaline phosphatase; promotes mineralization by degrading pyrophosphate | Classic marker of mineralization; not directly cited in provided list |
| SIBLING proteins (e.g., DMP1, DSPP) | Dentin matrix proteins involved in mineralization | Not directly cited in provided list but relevant to tooth mineralization |
| FGF23 | Regulates phosphate homeostasis; affects mineralization | Not directly cited in provided list but relevant to systemic mineralization |
| PHEX | Phosphate-regulating endopeptidase; mutations cause X-linked hypophosphatemia | Not directly cited in provided list but relevant to tooth mineralization |
| ENAM | Enamelin; enamel matrix protein | Not directly cited in provided list but relevant to enamel mineralization |
How Is positive regulation of tooth mineralization Regulated?
The positive regulation of tooth mineralization is controlled at multiple levels. At the transcriptional level, factors such as Trps1 regulate the expression of mineralization-related genes. At the post-transcriptional level, microRNA-21 facilitates osteoblast activity, thereby promoting mineralization. The circadian clock, through BMAL1/CLOCK, imposes a rhythmic pattern on mineralization, which is upstream-regulated by p75NTR [1,7]. Epigenetic regulation via KDM6B and metabolic pathways involving Pdk1 and ZEB2 lactylation drive cellular cementum formation. Additionally, osteoclast activity mediated by Ctsk+ cells influences condylar morphogenesis and indirectly affects mineralization. These layers of regulation ensure precise control of mineral deposition in teeth.
positive regulation of tooth mineralization and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| TRPS1 | Tricho-rhino-phalangeal syndrome with dental abnormalities | Trps1 knockout mouse; patient-derived iPSCs; CRISPR point mutation |
| AMELX | Amelogenesis imperfecta | Amelx knockout mouse; overexpression in ameloblast-like cells |
| NGFR (p75NTR) | Circadian rhythm disruption and mineralization defects | Ngfr knockout mouse; conditional knock-in of BMAL1/CLOCK |
| KDM6B/ZEB2 | Cementum defects and periodontal disease | Kdm6b or Zeb2 knockout mouse; overexpression of ZEB2 lactylation mutants |
| CTSK | Condylar morphogenesis and TMJ disorders | Ctsk knockout mouse; osteoclast-specific Cre models |
Tricho-Rhino-Phalangeal Syndrome and Dental Abnormalities
Mutations in TRPS1 cause tricho-rhino-phalangeal syndrome, an autosomal dominant disorder characterized by craniofacial and skeletal abnormalities, including dental defects. Trps1 regulates mineralization of dental tissues and proliferation of tooth organ cells, and its loss leads to impaired dental mineralization. This highlights the clinical importance of positive regulation of tooth mineralization in genetic syndromes.
Amelogenesis Imperfecta and Enamel Defects
Amelogenesis imperfecta is a group of inherited conditions affecting enamel formation. The amelogenin gene (AMELX) is critical for enamel mineralization, and its expression is developmentally regulated. Disruptions in positive regulation of tooth mineralization can lead to hypoplastic or hypomineralized enamel, increasing caries susceptibility. Understanding the regulators of amelogenin expression is essential for developing therapies.
Cementum Disorders and Periodontal Disease
Cellular cementum formation is essential for tooth root attachment and periodontal health. The KDM6B/Pdk1 glycolytic pathway-driven ZEB2 lactylation promotes cellular cementum formation. Dysregulation of this pathway could contribute to cementum defects, leading to tooth loss. Targeting this pathway may offer therapeutic strategies for periodontal regeneration.
Condylar Morphogenesis and Temporomandibular Joint Disorders
Ctsk+ osteoclasts orchestrate condylar morphogenesis via hypoxic lysosome. Abnormalities in this process can lead to temporomandibular joint disorders, including condylar resorption and osteoarthritis. Positive regulation of tooth mineralization intersects with bone remodeling in the condyle, highlighting the broader impact of mineralization regulators on craniofacial health.
From positive regulation of tooth mineralization-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does p75NTR promote tooth mineralization via BMAL1/CLOCK? | Ngfr knockout mouse; BMAL1/CLOCK knock-in; CRISPR knockout of Ngfr in odontoblasts |
| What is the role of Trps1 in dental mineralization? | Trps1 conditional knockout mouse; point mutation mimicking human TRPS1 mutations |
| How does microRNA-21 affect osteoblast activity and mineralization? | Mir21 knockout mouse; overexpression of miR-21 in osteoblasts; CRISPR knockout |
| Does KDM6B/Pdk1/ZEB2 pathway drive cementum formation? | Kdm6b or Zeb2 knockout mouse; knock-in of lactylation-deficient ZEB2; overexpression of Pdk1 |
| How do Ctsk+ osteoclasts influence condylar morphogenesis? | Ctsk-Cre; hypoxic lysosome inhibition; knockout of Ctsk in osteoclasts |
| What is the developmental regulation of amelogenin? | Amelx knockout mouse; tagged knock-in of AMELX; overexpression in ameloblasts |
How to Study the positive regulation of tooth mineralization Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Alizarin Red staining | Calcium deposits | Quantification of mineralized nodules in cell culture and tissue sections [1,4] |
| Micro-CT | Mineral density and 3D structure | Assessment of tooth and bone mineralization in animal models [6,8] |
| Fluorescent labeling (calcein) | Dynamic mineralization fronts | Analysis of incremental growth lines and rhythmic mineralization [1,7] |
| RNA-seq | Global gene expression | Identification of differentially expressed genes in mineralization models [4,6] |
| ChIP-seq | Transcription factor binding sites | Mapping of Trps1, BMAL1/CLOCK binding across genome [1,4] |
| Immunohistochemistry | Protein localization and expression | Detection of p75NTR, Trps1, ZEB2 in dental tissues [1,2,4,6] |
| Western blot | Protein abundance and modifications | Quantification of lactylation, phosphorylation |
| CRISPR knockout | Gene function | Generation of loss-of-function models for mineralization genes [1,4,6] |
Histological and Imaging Techniques for Mineralization
To study positive regulation of tooth mineralization, researchers use histological staining such as Alizarin Red and von Kossa to visualize calcium deposits [1,4]. Micro-computed tomography (micro-CT) provides quantitative assessment of mineral density in teeth and bone [6,8]. Fluorescent labeling with calcein or tetracycline allows dynamic monitoring of mineralization fronts and incremental lines [1,7]. These methods are essential for phenotyping knockout and transgenic models.
Transcriptomic and Epigenomic Profiling
RNA sequencing (RNA-seq) of dental tissues from wild-type and mutant animals reveals differentially expressed genes involved in mineralization [4,6]. Chromatin immunoprecipitation sequencing (ChIP-seq) can identify binding sites of transcription factors such as Trps1 and BMAL1/CLOCK [1,4]. Assay for transposase-accessible chromatin with sequencing (ATAC-seq) assesses chromatin accessibility changes during mineralization. These approaches uncover regulatory networks controlling positive regulation of tooth mineralization.
Protein and Post-translational Modification Analyses
Western blotting and immunohistochemistry are used to detect protein expression and localization of p75NTR, Trps1, ZEB2, and other regulators [1,2,4,6]. Lactylation of ZEB2 can be assessed by immunoprecipitation with anti-lactyl-lysine antibodies. Co-immunoprecipitation (Co-IP) identifies protein-protein interactions, such as p75NTR with BMAL1/CLOCK. These techniques elucidate molecular mechanisms.
Functional Assays in Cell Culture
Odontoblast-like cell lines (e.g., MDPC-23, OD-21) and primary dental pulp cells are used for in vitro mineralization assays [3,5]. Cells are cultured in mineralization-inducing medium, and mineral nodule formation is quantified by Alizarin Red staining. Overexpression or knockdown of candidate genes via lentiviral vectors or CRISPR interference (CRISPRi) allows functional validation. These assays complement in vivo models.
How CRISPR Can Be Used to Study GO:0070172 positive regulation of tooth mineralization
Knockout
CRISPR/Cas9-mediated knockout is widely used to study positive regulation of tooth mineralization. For example, Ngfr knockout mice have been generated to investigate the role of p75NTR in rhythmic mineralization. Trps1 knockout models recapitulate dental abnormalities seen in tricho-rhino-phalangeal syndrome. Knockout of Kdm6b or Zeb2 in mice impairs cementum formation. These models provide causal evidence for gene function in mineralization.
Point Mutation
Point mutations can be introduced using CRISPR base editors or homology-directed repair (HDR) to model human disease variants. For instance, specific TRPS1 mutations found in patients can be knocked into the mouse genome to study their impact on dental mineralization. Similarly, mutations in AMELX associated with amelogenesis imperfecta can be modeled. Point mutation models are valuable for understanding structure-function relationships.
Knock-in
Knock-in of reporter genes or tagged proteins allows visualization and tracking of mineralization regulators. For example, a BMAL1-luciferase knock-in mouse can be used to monitor circadian clock activity in real-time during tooth development. Tagged knock-in of ZEB2 with a lactylation-mimetic mutation can elucidate the role of lactylation in cementum formation. These models enable precise spatiotemporal analysis.
Overexpression
Overexpression of candidate genes via transgenic or viral vectors can test sufficiency in promoting mineralization. Overexpression of microRNA-21 in osteoblasts enhances osteoblast activity and mineralization. Overexpression of p75NTR or BMAL1/CLOCK in dental cells can increase mineral deposition. These gain-of-function studies complement loss-of-function approaches.
How EDITGENE Supports positive regulation of tooth mineralization Research
Researchers studying positive regulation of tooth mineralization-related genes often need to determine whether a candidate gene is causally involved in the process or merely correlated with it. EDITGENE provides a comprehensive suite of CRISPR-based services to generate precisely engineered cell and animal models, enabling rigorous functional validation of genes implicated in tooth mineralization.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of tooth mineralization research.
Related Products
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| WNT6 Knockout HEK293 Cell Line | EDJ-KQ119 | Human | 7475 | Details Get a Quote |
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| AMELX Knockout HeLa Cell Line | EDJ-KQ52606 | Human | 265 | Details Get a Quote |
| WNT6 Knockout HeLa Cell Line | EDJ-KQ54751 | Human | 7475 | Details Get a Quote |
| AMELX Knockout A-549 Cell Line | EDJ-KQ61085 | Human | 265 | Details Get a Quote |
| WNT6 Knockout A-549 Cell Line | EDJ-KQ63246 | Human | 7475 | Details Get a Quote |
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Frequently Asked Questions About positive regulation of tooth mineralization
What is GO:0070172 positive regulation of tooth mineralization?
GO:0070172 is a Gene Ontology biological process term defined as any process that activates or increases the frequency, rate or extent of tooth mineralization, the deposition of calcium salts in tooth structures [1,2].
What genes are involved in positive regulation of tooth mineralization?
Key genes include NGFR (p75NTR), BMAL1, CLOCK, TRPS1, AMELX, MIR21, KDM6B, PDK1, ZEB2, and CTSK, as identified in recent studies [1,2,3,4,5,6,7,8].
How does p75NTR regulate tooth mineralization?
p75NTR promotes tooth rhythmic mineralization by upregulating the circadian clock genes BMAL1 and CLOCK, linking circadian rhythm to incremental growth lines [1,7].
What is the role of Trps1 in dental mineralization?
Trps1 is a transcription factor that regulates mineralization of dental tissues and proliferation of tooth organ cells; mutations cause tricho-rhino-phalangeal syndrome with dental abnormalities.
How does microRNA-21 affect tooth mineralization?
MicroRNA-21 facilitates osteoblast activity, which indirectly promotes the formation of mineralized matrix in teeth.
What is the KDM6B/Pdk1/ZEB2 pathway in cementum formation?
This pathway involves KDM6B and Pdk1-driven glycolysis leading to ZEB2 lactylation, which promotes cellular cementum formation, a key component of tooth root attachment.
What diseases are associated with defects in tooth mineralization?
Diseases include tricho-rhino-phalangeal syndrome (TRPS1 mutations), amelogenesis imperfecta (AMELX mutations), and periodontal disease related to cementum defects [4,5,6].
How can CRISPR be used to study positive regulation of tooth mineralization?
CRISPR knockout, point mutation, knock-in, and overexpression models allow researchers to test the causal role of specific genes in mineralization processes [1,4,6].
What methods are used to measure tooth mineralization?
Common methods include Alizarin Red staining, micro-CT, fluorescent labeling, RNA-seq, ChIP-seq, and immunohistochemistry [1,4,6,8].
What is the role of Ctsk+ osteoclasts in condylar morphogenesis?
Ctsk+ osteoclasts orchestrate condylar morphogenesis via hypoxic lysosome, influencing temporomandibular joint development and indirectly affecting mineralization.
Conclusion
GO:0070172 positive regulation of tooth mineralization encompasses a complex network of molecular regulators, including p75NTR, Trps1, microRNA-21, and the KDM6B/Pdk1/ZEB2 pathway. These factors ensure proper deposition of calcium salts in enamel, dentin, and cementum, and their dysregulation leads to dental and craniofacial disorders. Continued research using CRISPR-based models and advanced imaging will further elucidate these mechanisms and inform regenerative strategies. EDITGENE stands ready to support these efforts with tailored gene editing services.
References
- 1. Xie B et al.. 2023. p75NTR promotes tooth rhythmic mineralization via upregulation of BMAL1/CLOCK.. Front Cell Dev Biol 11:1283878 PMID: 38020910
- 2. Zhao M et al.. 2019. The spatiotemporal expression and mineralization regulation of p75 neurotrophin receptor in the early tooth development.. Cell Prolif 52(1):e12523 PMID: 30357966
- 3. Oka S et al.. 2021. MicroRNA-21 facilitates osteoblast activity.. Biochem Biophys Rep 25:100894 PMID: 33426313
- 4. Goss M et al.. 2019. Trps1 transcription factor regulates mineralization of dental tissues and proliferation of tooth organ cells.. Mol Genet Metab 126(4):504-512 PMID: 30691926
- 5. Chen E et al.. 1994. Regulation of amelogenin gene expression during tooth development.. Dev Dyn 199(3):189-98 PMID: 8018986
- 6. Yang Z et al.. 2026. KDM6B/Pdk1 glycolytic pathway-driven ZEB2 lactylation promotes cellular cementum formation.. Int J Oral Sci 18(1) PMID: 41771827
- 7. Yuan H et al.. 2022. A potential role of p75NTR in the regulation of circadian rhythm and incremental growth lines during tooth development.. Front Physiol 13:981311 PMID: 36213234
- 8. Tang Y et al.. 2026. Ctsk(+) Osteoclasts Orchestrate Condylar Morphogenesis via Hypoxic Lysosome.. J Dent Res 105(5):626-636 PMID: 41108121
