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)
Ask about this productRelated 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)
- Alzheimer's disease (AD) is a neurodegenerative disorder causing progressive neuronal damage. Incidence rises with age, and early diagnosis is difficult. This study examined DLX6-AS1 clinical relevance and regulatory mechanism in AD, and its interaction with miR-204-5p in AD pathology. It offers new insights into early diagnosis and treatment. A total of 133 AD patients and 105 healthy controls were selected. Their serum levels of DLX6-AS1 and miR-204-5p were analyzed using quantitative polymerase chain reaction. β-amyloid (Aβ)-induced SH-SY5Y neuronal injury and okadaic acid (OA)-induced Neuro-2a tau abnormal phosphorylation models were constructed. The role/function of DLX6-AS1/miR-204-5p axis was then investigated using cell counting kit-8, flow cytometry, western blotting, enzyme-linked immunosorbent assay and a dual-luciferase reporter gene assay. AD patients had higher serum DLX6-AS1 and lower miR-204-5p levels. DLX6-AS1 showed an AUC of 0.838 for AD diagnosis. DLX6-AS1 levels were negatively associated with cognitive function, brain structural integrity, and benign pathology-and positively associated with disease severity, functional impairment, and pathological markers. In AD cell models, DLX6-AS1 was upregulated. Silencing it promoted cell proliferation, reduced apoptosis and oxidative stress, improved mitochondrial and synaptic function, decreased tau phosphorylation, and enhanced microtubule stability and axonal transport. Dual-luciferase assays confirmed direct binding between DLX6-AS1 and miR-204-5p. Co-inhibition reversed the protective effects of DLX6-AS1 silencing. Serum DLX6-AS1 is a potential biomarker for early diagnosis and assessment of AD. It regulates Aβ-induced neuronal damage and tau phosphorylation by targeting miR-204-5p, offering a new mechanism target for AD molecular therapy. - Source: PubMed
Publication date: 2026/07/29
Jiang MinggangLin YangWang LipingOu Kaiyun - Distal-less homeobox genes Dlx5 and Dlx6 are key regulators of osteoblast differentiation during skeletal development, but their role in postnatal bone remodeling remains poorly understood. To investigate this, we conditionally deleted Dlx5/6 in Osterix-lineage cells after 4 weeks of birth using an inducible Osx-Cre system. Dlx5/6Δ/Δ Osx-Cre and control mice were analyzed in terms of bone architecture (micro-computed tomography), remodeling (histomorphometry), gene expression profiling and single-cell RNA sequencing. Postnatal deletion of Dlx5/6 induced a complex skeletal phenotype characterized by radial bone hypertrophy and altered cortical remodeling. Enhanced periosteal activity was associated with increased Osx expression in periosteal cells, confirmed by BaseScope and immunofluorescence analyses. In parallel, cortical bone became thinner and more porous, while trabecular bone displayed reduced bone formation and thinner trabeculae, despite paradoxical accumulation within the diaphysis. These alterations were associated with increased Osx expression in periosteal and diaphyseal compartments, indicating abnormal spatial regulation of osteolineage cell expansion and bone remodeling. Single-cell transcriptomic analysis in bone-marrow cells identified altered mesenchymal stromal cell populations with dysregulated extracellular matrix and Wnt signaling pathways, including downregulation of the Wnt antagonist Sfrp1, validated in situ by RNAscope. Consistently, osteoblasts derived from Dlx5/6Δ/Δ Osx-Cre displayed impaired terminal differentiation in vitro, with reduced expression of late osteogenic markers and decreased matrix mineralization. Collectively, these findings identify Dlx5/6 as critical regulators of postnatal bone homeostasis that coordinate osteolineage expansion and terminal osteoblast maturation during postnatal bone remodeling. - Source: PubMed
Publication date: 2026/07/21
Bourmaud MorganeNarboux-Neme NicolasZarka MylèneBlandin CamilleMella SebastienLibri ValentinaHasan MilenaHay EricLevi GiovanniCohen-Solal Martine - Lung adenocarcinoma (LUAD) is a leading cause of cancer-related mortality worldwide, with limited treatment options due to inherent chemotherapy resistance. Ferroptosis, an iron-dependent form of regulated cell death, has recently emerged as a promising strategy to overcome this resistance. Inducing ferroptosis may sensitize LUAD cells to chemotherapy, but its molecular regulators and therapeutic potential remain largely unexplored. This study aims to investigate the role of Distal-less homeobox 6 (DLX6) in regulating ferroptosis and its contribution to LUAD progression. - Source: PubMed
Publication date: 2026/07/15
Sun ZedongZhou MinminWang CanLiu MingruiSong NingdanHe SimianJi FeifanChen JiayuXu LinZheng XiufenRen Binhui - Cervical cancer remains a major worldwide health concern and ranks as the fourth most common malignancy affecting women, especially in low- and middle-income countries, where early screening and monitoring facilities are limited. Though several screening strategies, including Pap smears, colposcopy, computed tomography, and HPV testing, are available for the detection of cervical carcinoma, these methods cope with various challenges, such as diagnostic errors, false-positive and false-negative results, invasiveness, and sample collections, which could lead to unnecessary anxiety and procedures. Recent studies suggest that extracellular vesicles (EVs) are emerging as a promising noninvasive diagnostic and prognostic tool for early detection of cervical cancer. EVs are secreted by almost all types of cells, including tumor cells, into various biofluids and carry molecular signatures reflective of their cells of origin. EVs exhibit stability in circulation due to their protective lipid bilayer and are enriched with nucleic acids, proteins, and lipids that serve as potential biomarkers. Particularly, tumor-derived EVs from tissues, plasma, urine, and vaginal secretions have demonstrated diagnostic value in cervical cancer by carrying oncogenic miRNAs, lncRNAs, miR-221-3p, and proteins such as DLX6-AS1 and survivin. Furthermore, EVs contribute to cancer by immune modulation, metastasis, and treatment resistance, underscoring EVs' diagnostic and prognostic potential. Compared to conventional liquid biopsies, EVs provide enhanced biomarker stability and specificity. This review highlights the biogenesis, isolation methods, functional role, and clinical significance of EVs, and their integration into cervical cancer screening and management strategies. - Source: PubMed
Wahid AmirMaharaj RayMeiring MurielAnand Krishnan - The DNA binding domains of transcription factors are structurally well-defined and their presence in novel genome sequence can be reliably detected via sequence homology. In contrast, regions of transcription factors that stimulate or repress mRNA synthesis by RNA polymerase II are more enigmatic and difficult to identify with bioinformatic tools. Experimental discovery of transactivation (or repression) domains typically makes use of a reporter gene transcription assay in one or more cell types and the progressive removal of protein sequence from the transcription factor under study. By and large, this reveals one or more minimal subdomains that are required for most of the transcription activity for the wild type protein. In applying this approach to the experimental identification of minimal transactivation domains of the chicken DLX5 and DLX6 paralogues, we find no obvious subdomain organization but, instead, show redundant transactivation activity that is distributed throughout each protein. We also reveal that DLX domains can cooperate in trans in homo- or heterotypic reactions with DLX domains that are DNA-bound via the homeodomain. - Source: PubMed
Publication date: 2026/06/30
Samifanni RojinaBendall Andrew J