HOXA4 EMSA Probe Set
- Known as:
- HOXA4 EMSA Probe Set
- Catalog number:
- AY1326P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- HOXA4 EMSA Probe Set
Related genes to: HOXA4 EMSA Probe Set
- Gene:
- HOXA4 NIH gene
- Name:
- homeobox A4
- Previous symbol:
- HOX1D, HOX1
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2014-11-19
Related products to: HOXA4 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: HOXA4 EMSA Probe Set
- HOX genes encode transcription factors that are central regulators of cell fate during embryogenesis and of maintaining respective positional cell identity throughout life. Moreover, HOX factors shape the specification of regional properties of the respective tissues, but detailed information regarding the role of HOX genes in the adult human respiratory system is still lacking. - Source: PubMed
Publication date: 2026/07/14
Budeus BettinaKlein Diana - Microtia-atresia is a rare craniofacial malformation primarily affecting the first and second pharyngeal arches, leading to the deformity of the auricle and atresia of the external ear canal. Its etiology is heterogenous and largely unknown, including both genetic and environmental factors. The gene has been identified as potentially pathogenetic for microtia-atresia in three twin families. A mosaic knockdown zebrafish model was constructed using CRISPR/Cas9. was expressed in the mandible during early development in zebrafish, while the F0 mosaic knockdowns exhibited craniofacial malformations with abnormal chondrocyte morphologies. Specifically, knockdown reduced cranial neural crest cell proliferation while increasing apoptosis, markedly downregulating chondrogenic markers and . Consequently, pharyngeal arch chondrocytes exhibited disorganized arrangement and morphological abnormalities, resulting in mandibular hypoplasia. Our findings provide important insights into the role of in zebrafish mandibular development and the pathology of microtia-atresia caused by gene mutations in humans. - Source: PubMed
Publication date: 2026/05/15
Sun LePing LuZhang FuyuGao RuzhenZhang BoChen Xiaowei - Human amniotic membrane mesenchymal stem cells (hAMSCs) hold strong cardioprotective potential, yet their mechanisms of action remain largely elusive. - Source: PubMed
Alcharani NunzioTesoro LauraDÃez-Mata JavierZamorano José LuisSaura MartaIglesias MaiteZaragoza Carlos - KIF11 is a mitotic kinesin responsible for the formation and maintenance of bipolar spindles, and it has high expression in the hepatocellular carcinoma (HCC). However, the role of the KIF11 gene in the hepatitis B virus (HBV)-related HCC remains unknown. Thus, this study aims to explore the function of transcription factor HOXA4 binding to KIF11 in HBV-related HCC, with the goal of providing a novel gene therapy approach for its treatment. HBV-positive (HepG2.2.15 cells) and HBV-negative (HepG2 cells) liver cancer cells were used to investigate the expression of KIF11 and HOXA4. HepG2 cells or HepG2.2.15 cells were transfected with the pc3.1-HBx, si-KIF11, and si-HOXA4, or co-transfected with the si-HOXA4 and oe-KIF11 for subsequent analysis. The binding of HOXA4 protein to the KIF11 gene promoter was examined based on a ChIP assay. The characteristics of HepG2.2.15 cells and HepG2 cells were assessed using CCK-8 and flow cytometry. HBV transcription and replication levels were detected via Northern and Southern blotting. The secretion level of HBV antigens in the HepG2.2.15 cell supernatant was measured by ELISA. KIF11 and HOXA4 were highly expressed in the HepG2.2.15 cells. Silencing KIF11 inhibited cell viability and HBV replication and transcription, reduced HBsAg and HBeAg levels in cell supernatants, promoted apoptosis, and downregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2.2.15 cells. pc3.1-HBx promoted cell viability, inhibited apoptosis, and upregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2 cells, which was reversed by si-KIF11. ChIP assays confirmed that HOXA4 bound to the KIF11 gene promoter. Silencing HOXA4 suppressed cell viability and HBV replication and transcription, decreased HBsAg and HBeAg levels in cell supernatants, enhanced apoptosis, and downregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2.2.15 cells. Silencing HOXA4 inhibited cell viability, promoted apoptosis, and downregulated p-PI3K/PI3K and p-AKT/AKT protein expression in HepG2 cells with pc3.1-HBx transfection. Overexpression of KIF11 counteracted the effects of si-HOXA4 in the HepG2.2.15 cells or HepG2 cells with pc3.1-HBx transfection. In conclusion, silencing of HOXA4 inhibited HBV replication and HCC proliferation by downregulating KIF11, providing a novel gene-assisted therapeutic approach for HBV-related HCC. - Source: PubMed
Publication date: 2026/02/12
Ma JinlingLiao Duodi - Transcranial magnetic stimulation (TMS) is an established treatment for major depressive disorder (MDD), yet response rates remain suboptimal and biomarkers predictive of treatment outcomes are currently lacking. Recently, DNA methylation (DNAm) has shown promise as an epigenetic predictor of antidepressant and electroconvulsive therapy treatment outcomes but no study to our knowledge has characterized DNAm profiles of treatment outcomes in the context of TMS. Here, we present the first genome-scale DNAm analysis of TMS outcomes in patients with treatment-resistant depression (TRD). - Source: PubMed
Publication date: 2025/11/12
Dahrendorff JanPages KennethCurrier GlennSarker Mainul HasanGraham ZacharyLouis-Jacques Adetola FDagne GetachewUddin Monica