TWIST2
- Known as:
- TWIST2
- Catalog number:
- 000487A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- TWIST2
Related genes to: TWIST2
- Gene:
- TWIST2 NIH gene
- Name:
- twist family bHLH transcription factor 2
- Previous symbol:
- -
- Synonyms:
- DERMO1, Dermo-1, bHLHa39
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-25
- Date modifiied:
- 2015-09-08
Related products to: TWIST2
Related articles to: TWIST2
- ObjectiveGenome-wide association studies have identified over 80 loci associated with nonsyndromic orofacial cleft (NSOC), yet substantial heritability remains unexplained. Insights from syndromic orofacial cleft (SOC) implicated genes could help bridge this gap.DesignA case-control association study in a Han Chinese cohort was conducted to evaluate the association between SOC-implicated genes and NSOC subtypes using association, linkage disequilibrium (LD), and haplotype analyses.SettingTertiary medical center.Patients, ParticipantsThe study included 1626 cases of non-syndromic cleft lip with or without cleft palate, 930 cases of non-syndromic cleft palate only, and 2255 controls.InterventionsPeripheral blood (cases) and umbilical cord blood (controls) were collected for DNA extraction.Main Outcome MeasuresAllelic (Pearson' s , 1 df) and genotypic (Pearson' s , 2 df) associations between SNPs and NSOC subtypes were evaluated, with odds ratios (ORs) and 95% confidence intervals (CIs). LD and sliding-window haplotype association analyses were performed in Haploview. SNPs with minor allele frequency (MAF) >0.05 and in Hardy-Weinberg equilibrium in controls were analyzed. The significance threshold was < 1.27 × 10 after Bonferroni correction.ResultsAllelic analysis identified 23 SNPs that were significantly associated with NSOC subtypes (lowest = 2.02 × 10). Genotypic analysis identified 39 significant SNPs (lowest = 1.09 × 10). Signals mapped to 7 genes. Haplotype analyses revealed a shared causal variant block at and , and allelic heterogeneity at .ConclusionsWe identified , , and as NSOC-associated genes. Using SOC genes as prior knowledge reveals loci missed by standard GWAS, offering key insights into NSOC pathogenesis. - Source: PubMed
Publication date: 2026/05/04
You YueLin Yan-SongJia Si-XuanZhang Si-DiSun Jia-LinShi BingJia Zhong-Lin - - Source: PubMed
Publication date: 2026/04/06
Zeng TaoZhang LingYin WenxinYou CuipingLilljebjörn HenrikWang QianZhang WeinaJi XiaotianWang YuliangLiu YongjingXie YaliFeng XiaoxiZhang XiangJiang HuaFioretos ThoasXiao GangJin JieChen SuningHuang Jinyan - It is widely accepted that Taste bud cells originate from the epithelium; however, evidence indicates that these cells are also derived from the mesenchyme beneath the epithelium. In this study, the cell lineage expressing Twist2, a transcription factor that is specifically expressed in the mesenchyme within taste buds, were examined to gain a deeper understanding of its biological characteristics. - Source: PubMed
Publication date: 2025/12/30
Takaku-Tanoue NamikiMatsuyama KaeToyono TakashiKataoka ShinjiNakatomi MitsushiroTakai ShingoShigemura NoriatsuKawamoto TatsuoSeta Yuji - Regenerative endodontics aims to restore the damaged pulp-dentin complex, moving beyond revascularization to functional tissue regeneration, which includes innervation. While dental pulp stem cells (DPSCs) have been widely studied, their clinical application is hindered by low cell yield and reduced regenerative capacity in late passages. This study investigates the feasibility of using Wharton's Jelly mesenchymal stem cells (WJ-MSCs) as an alternative allogenic cell source, combining them with a decellularized human dental pulp (dDP) scaffold as a platform crucial for functional pulp regeneration. Dental pulp tissues were successfully decellularized, confirmed by DNA and hydroxyproline quantification, and histological and SEM analyses showing robust preservation of collagen types I and III with efficient cell removal. WJ-MSCs were then successfully repopulated onto the dDP scaffolds, demonstrating cellular attachment and migration into the ECM. Repopulated dDP constructs exhibited a propensity for osteogenic and odontogenic differentiation, evidenced by Alizarin Red staining for mineral deposition and upregulated gene expressions of osteogenic (DLX5, OSTERIX) and odontogenic (DSPP) markers. Furthermore, neurogenic marker NCAM was upregulated, whereas inhibitory genes (TWIST2, MSX1), angiogenic markers (VE-CADHERIN, VEGF), and immune regulatory marker IDO1 were downregulated following differentiation. Overall, the findings suggest the feasibility of combining WJ-MSCs with dDP scaffolds as a novel approach for functional pulp regeneration, offering a promising pathway for future clinical translation in regenerative endodontics. - Source: PubMed
Publication date: 2026/02/12
Mohd Noor Nora SakinaLam Xin-JiehLim Ghee-SeongLau May-NakWey Mang-ChekRajendran AbilashiniThen Khong-LekHaque NazmulKasim Noor Hayaty AbuGovindasamy VijayendranAzami Noor Hayati - Alternative splicing (AS) is a key driver of transcriptomic diversity and plays a pivotal role in epithelial-mesenchymal transition (EMT). During EMT, dynamic splicing changes contribute to cell plasticity and metastasis, yet the upstream regulatory logic remains unclear. Although transcription factors (TFs) are thought to influence AS programs, they typically act through RNA-binding proteins (RBPs), forming a hierarchical TF$\rightarrow $RBP$\rightarrow $AS cascade. Current computational strategies struggle to recover such multi-layered regulation from bulk cross-sectional data, limiting our ability to identify TFs that ultimately control EMT-related AS events. To address this gap, we developed CTAS, a network control theory-based approach to identify key regulatory TFs of AS events during EMT. CTAS integrates pseudotime ordering, trend analysis, sparse directed network inference, and control-theoretic screening into a unified framework. In simulations, CTAS reconstructs EMT trajectories with Spearman's $\rho = 0.99946$ and directed networks with ROC AUC = 89.9%, and remains robust under noise. Applied to a TCGA BRCA cohort, CTAS builds a directed TF$\to $RBP$\to $AS network and identifies HOXA3 (1.00), PRDM8 (0.86), and TWIST2 (0.83) as top TF controllers, alongside significant dynamic shifts in nine AS events detected by Wilcoxon test ($P <.05$). A focused CD44 subnetwork further highlights ZNF521 (0.86) and HIC1 (0.65) as candidate regulators. These findings demonstrate that CTAS transforms cross-sectional data into dynamic regulatory insights and yields experimentally testable TFs that control AS during EMT. - Source: PubMed
Gan YanHe YangsongZhao PuChing Wai-KiQiu Yushan