Dlx6 antibody - C-terminal region (ARP35763_P050)
- Known as:
- Dlx6 (anti-) - C-terminal region (ARP35763_P050)
- Catalog number:
- arp35763_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Dlx6 antibody - C-terminal region (ARP35763_P050)
Related genes to: Dlx6 antibody - C-terminal region (ARP35763_P050)
- Gene:
- DLX6 NIH gene
- Name:
- distal-less homeobox 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-24
- Date modifiied:
- 2016-04-25
Related products to: Dlx6 antibody - C-terminal region (ARP35763_P050)
Related articles to: Dlx6 antibody - C-terminal region (ARP35763_P050)
- Rett syndrome is a severe neurodevelopmental disorder caused predominantly by loss-of-function mutations in the X-linked gene . In addition to a vast array of neurological and physiological impairments, patients also frequently develop severe osteopenia with increased fracture risk; however, the mechanisms underlying these skeletal defects are not completely understood. Previous work in -null mouse models has suggested that osteopenia is mainly due to impaired osteoblast function and reduced bone formation. Here, we examined bone mass, microarchitecture, and remodeling parameters in a -null mouse model during postnatal development, with a particular focus on osteoclast involvement. Microcomputed tomography and histomorphometric analyses showed reduced bone mineral density and trabecular bone volume, which are associated with increased trabecular separation and cortical thinning. These structural alterations were accompanied by increased osteoclast number per bone surface, elevated urinary deoxypyridinoline, and higher expression of osteoclast-associated genes, including . Furthermore, gene expression analysis revealed an age-dependent shift in bone remodeling. At postnatal day 35, mutant mice showed reduced expression of and , consistent with low bone turnover. By postnatal day 55, and were markedly upregulated, suggesting an increase in osteoclast resorptive activity, while key osteoblast markers and the RANKL/OPG ratio did not change significantly. A potential cell-autonomous contribution of to osteoclast maturation is also suggested by the analysis of public transcriptomic datasets on human osteoclast differentiation. Together, our findings identify increased osteoclast activity as a significant contributor to Rett-associated osteopenia and suggest that skeletal pathology in deficiency progresses from an early low-turnover state to a later phase of increased osteoclast resorption. - Source: PubMed
Publication date: 2026/05/21
Samee NadeemBelz LouNarboux-Nême NicolasRoux Jean-ChristophePanayotis NicolasLevi Giovanni - Wilms tumor (WT) is a frequently diagnosed cancer in pediatric patients. DLX6-AS1 contributes to the emergence of several cancers. Nonetheless, the role of DLX6-AS1 in WT remains unclear. This study aimed to explore potential mechanisms by which DLX6-AS1 promotes the progression of WT. - Source: PubMed
Publication date: 2026/05/19
Chen JiaweiLi GuoweiChen LuqiuLi YunfengSun Fengyin - This study aimed to evaluate the effect of lncDlx6os1 on high glucose (HG)-induced oxidative stress and the involvement of the parkin pathway. - Source: PubMed
Diao JiayuGou QilingZhang LintingWu FengchaoLiang Lei - Tooth dentin, secreted by odontoblasts, constitutes most of the tooth structure and provides support and sensory function. However, dentin defects are common and irreparable once they exceed a critical threshold. Human dentin develops from dental papilla (DP) cells under the guidance of the dental epithelium (DE). Here, we present a human tooth development atlas from initiation to erupted stage using single-cell RNA sequencing and spatial transcriptomics, focusing on epithelial-mesenchymal interactions. This atlas reveals that DE orchestrates DP differentiation in a WNT-NOTCH sequential activation model and identifies the key signaling molecules. DLX6-AS1 DP cells respond to dental epithelial signals and can be isolated from adult dental pulp stem cells (DPSCs). Notably, DLX6-AS1 DPSCs successfully generate tubular dentin in an in vivo disease model of dentin defects. This research provides valuable information on human tooth development and establishes a basis for repairing regenerative dental tissue. - Source: PubMed
Publication date: 2026/02/14
Wei WeiWu ChuanSun JingHan MengjieGu XiugeZhou HanzhangWu XiaoshanShen ZongshanZhang ChunmeiWang JinsongHu LeiLuo LanrongZhang YuanyuanHu LinaWang SonglinZhang Ran - This study explores the cell fate reprogrammability of H3K27M-mutant pediatric high-grade gliomas (pHGG) using neuronal transdifferentiation as a potential targeted therapy. We treated the BT245 patient-derived glioma cell line with pharmacological combinations targeting neuronal differentiation pathways and performed bulk RNA sequencing to characterize gene expression patterns driving cell fate transitions. Our findings reveal that the drug combinations induce transcriptomic changes consistent with differentiation towards neuronal phenotypes, including the upregulation of synaptic and dendritic signaling genes and the downregulation of malignant signatures. In comparison, astrocytic differentiation media (DM) and H3K27M knockout (KO) promote residual astrocytic phenotypes, suggesting neuronal transdifferentiation as a more effective strategy for mitigating tumor aggressiveness and progression. Differentially expressed genes such as GRIK1, GRIN1, NRXN3, NRXN1, CALB2, SCGN, SLC32A1, SLC1A2, KCNC3, and neurodevelopmental regulators including WNT7A, DLX6, ERBB4, ARX, BCL11B, SEMA3C, and FGFBP3 were identified as key markers regulating the neuron-like lineage transition. This study demonstrates that pHGGs can be phenotypically redirected toward neuronal-like identities through modulating cell fate differentiation programs. These findings advance the concept of 'differentiation therapy' as a promising intervention to reduce phenotypic plasticity and malignancy in pHGG ecosystems. While these are early in vitro findings, the potential ability to steer and control glioma cells toward stable, less malignant fates offers promising translational potential for patient-centered targeted therapies. - Source: PubMed
Publication date: 2025/12/30
Uthamacumaran AbicumaranHorth CynthiaBareke EricGravel MichelMajewski Jacek