PITX2 Western Blot kit other
- Known as:
- PITX2 Western Blot reagent other
- Catalog number:
- 'AWBK35634
- Product Quantity:
- 1 kit
- Category:
- -
- Supplier:
- ACR
- Gene target:
- PITX2 Western Blot kit other
Ask about this productRelated genes to: PITX2 Western Blot kit other
- Gene:
- PITX2 NIH gene
- Name:
- paired like homeodomain 2
- Previous symbol:
- IRID2, IHG2, RIEG, RIEG1, RGS
- Synonyms:
- IGDS, RS, Brx1, Otlx2, ARP1
- Chromosome:
- 4q25
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-05
- Date modifiied:
- 2016-01-27
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- Topologically associating domains (TADs) are fundamental units of three-dimensional genome organization, and their boundaries play important roles in gene regulation and genomic stability. However, accurate computational prediction of TAD boundaries remains challenging because of the complex interplay between DNA sequence and epigenomic regulatory signals. Here we present CT-TADB, a hybrid CNN-Transformer framework that integrates DNA sequence with histone modification and CTCF binding signals to predict TAD boundaries without requiring Hi-C data. Trained on six human cell lines, CT-TADB achieved AUC values of 0.932-0.950, demonstrating competitive or superior performance relative to existing multi-modal methods. The model maintained stable performance on strictly independent and dataset-specific boundary subsets, and exhibited robust cross-cell-type transferability and cross-species generalization between human and mouse (AUC > 0.80 for human-to-mouse transfer). Feature attribution analysis identified CTCF as the dominant boundary-associated factor, supported by active chromatin marks, and quantitative attention analysis revealed significant long-range CTCF-mediated dependencies (p < 0.001). CT-TADB further identified a clinically validated PITX2-associated TAD boundary linked to cardiac arrhythmia and captured condition-specific boundary dynamics. By leveraging routinely available epigenomic data, CT-TADB provides a practical and complementary framework for investigating chromatin architecture across diverse biological contexts. - Source: PubMed
Publication date: 2026/05/09
Chen TongWang ShuaibinJin YuyuYuan YuanLiang ZhenShen Yin - Early-stage diagnosis of paroxysmal atrial fibrillation (PAF) is challenging owing to its asymptomatic nature. However, the genetic factors underlying PAF and predictive utility of polygenic risk scores (PRSs) for PAF in Asian populations remain elusive. We aimed to explore the PAF-associated genetic variants in a Japanese cohort and evaluate the predictive performance of PAF-specific PRSs. This study included 2,604 participants. Following exclusion, quality control, and genotype imputation, a genome-wide association study (GWAS) was conducted. The predictive performance of 30 sets of PRS models constructed across various thresholds was evaluated using three machine learning methods. Model performance was assessed using area under the curve (AUC) and SHapley Additive exPlanations (SHAP). The GWAS using 1,038 PAF cases and 744 controls identified 82 genome-wide significant variants (P < 5 × 10-8), all on chromosome 4q25. Of these, 80 variants clustered upstream of PITX2, and two were located in LINC01438. Fine mapping identified two independent intergenic signals, with rs2200732 as the lead single-nucleotide polymorphism. The best PRS-only model achieved an AUC of >0.70, which was improved up to 0.737 in additive models incorporating both PRS and clinical variables. SHAP analysis consistently ranked PRS as the most influential predictor among the clinical variables included in this study. These results suggest that genetic risk, particularly at the established 4q25/PITX2 locus, contributes substantially to PAF susceptibility in this Japanese cohort and that PRS may improve early risk stratification when integrated with clinical risk factors. - Source: PubMed
Publication date: 2026/05/04
Shiomi MegumiNagata YukiSudo TakeakiTakahashi KentaroHiguchi ChihiroIhara KensukeAsada KenTanaka YasuakiYamauchi YasuteruSasaki TakeshiHachiya HitoshiImai YasushiFujita HideoSasano TetsuoFurukawa TetsushiTanaka Toshihiro - ADAMTS1 (a disintegrin-like and metalloproteinase domain with thrombospondin type 1 repeats) is a secreted metalloproteinase with a known role in extracellular matrix remodeling in cardiovascular development and female fertility. Because of conflicting report of embryonic lethality and survival in mutant mice, we report generation and characterization of a new knockout (KO) allele, which led to detection of neonatal lethal omphalocele (persistent umbilical hernia) as a new -dependent birth defect. This phenotype was also detected in another mutants with an in-frame insertion. β-galactosidase staining in the latter showed that was strongly expressed in the undifferentiated cells in the developing ventral abdominal wall preceding midline fusion at the umbilical cord attachment site. The omphalocele was characterized by the accumulation of the proteoglycan versican along with reduced proteolysis and impaired development of the superficial muscle layer, the panniculus carnosus, around the site of umbilical cord attachment. Furthermore, we observed sustained expression of the transcription factor, paired-like homeodomain transcription factor 2 in KO embryos, whereas it was downregulated in wild-type embryos during late embryogenesis. ADAMTS1 is thus a new matrisome component required for body wall closure. - Source: PubMed
Publication date: 2026/04/28
Opoku GabrielIkemura KentaroHatipoglu Omer FOhtsuki TakashiSato IkumiTaniguchi HibikiSakamoto ShinoHasib FarhanaWatanabe ShogoMead Timothy JApte Suneel SHirohata Satoshi - Anorectal malformation (ARM) is the most common congenital digestive tract anomaly in newborns, and children with ARM often have varying degrees of underdevelopment of the pelvic floor muscles (PFMs). To explore the effects of Rarα (NR1B1) and Pitx2 on the development of rat PFMs, we constructed a rat ARM animal model using all-trans retinoic acid (ATRA), and verified the expression of Rarα and Pitx2 in the PFMs of fetal rats. Additionally, we used rat myoblasts (L6 cells) to investigate the regulatory roles of Rarα and Pitx2 in skeletal muscle myoblast differentiation and their interactions. The results indicated a significant decrease in the expression of Rarα and Pitx2 in the PFMs of fetal rats with ARM. ATRA can also decrease the expression of Rarα and Pitx2 in the L6 cells, while affecting the differentiation and fusion of L6 cells. Knocking down Rarα in L6 cells reduced the expression of Pitx2, Myod1, Mymk, and decreased myogenic activity in L6 cells. When Rarα is activated, the decreased expression of Pitx2, Myod1, and Mymk and myogenic differentiation can be restored to different extents. At the same time, increasing or inhibiting the expression of Pitx2 can counteract the effects of knocking down Rarα and activating Rarα respectively. These results indicate that Pitx2 may be downstream of the transcription factor Rarα, mediating the effects of ATRA on the development of fetal rat PFMs. - Source: PubMed
Publication date: 2026/04/17
Zhao HanbinCao JianMu HuaqiBi YangGuo ZhenhuaShi YuanWang Yi - Multiple mouse lines using constitutive or inducible Cre recombinase expression have taken advantage of the early optic field expression of the Rax/Rx gene and its subsequent, progressive restriction to retinal progenitors, RPE, and the optic stalk. Among these, the constitutive transgenic lines, Rx3-Cre and Rax-Cre BAC Tg, are currently used by vision researchers. Here we directly compare their prenatal ocular and extraocular Cre activities. - Source: PubMed
Brown Nadean LGoodyear-Brown SamuelFuhrmann Sabine