NKX3-2 antibody - middle region (ARP33200_P050)
- Known as:
- NKX3-2 (anti-) - middle region (ARP33200_P050)
- Catalog number:
- arp33200_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NKX3-2 antibody - middle region (ARP33200_P050)
Related products to: NKX3-2 antibody - middle region (ARP33200_P050)
Related articles to: NKX3-2 antibody - middle region (ARP33200_P050)
- Whereas ligaments hold skeletal elements together, tendons bridge the musculature with the skeleton. How connective tissues of the right type and function are specified in distinct regions of the developing body remains unclear. Here, we have generated single-cell datasets of RNA expression and chromatin accessibility for scxa:mCherry+ connective tissues of the developing zebrafish face. We identified cell clusters corresponding to tendon, ligament, periligament, perichondrium and other types, as well as tendon and ligament subtypes with an osteogenic signature that may explain the remodeling of ligament-bone interfaces and the formation of sesamoid bones. We further identified several enhancers driving spatially restricted transgenic activity in ligaments, periligament tissue and other connective tissues. By utilizing a ligament-specific photoconvertible nlsEOS transgenic line, we revealed directional growth of ligaments. In addition, we found that nkx3.2 is expressed within the joint-proximal domain of the major jaw-stabilizing ligament, with this domain being lost in nkx3.2 mutants. Our study reveals distinct gene regulatory programs for jaw connective tissue diversification and provides a mechanism underlying the propensity of tendons and ligaments to ossify in normal and pathological contexts. - Source: PubMed
Publication date: 2026/02/05
Roberts Ryan RBhojwani ArshiaTseng Kuo-ChangElliott KelseyChen Hung-JhenTeubner LaurenSherwood DesmarieSmeeton JoannaMiller Cameron LNayak Pavan KSubramanian ArulSchilling Thomas FMerrill Amy ECrump J Gage - To identify the expression of Nkx3.2 in retinal pigment epithelium (RPE) and evaluate its physiological role in association with retinal degeneration. - Source: PubMed
Park MinsunChoi Seung-WonJeong Da-UnShin Hae-SolHan JiyeonOh Hye-KyoungJang Jun-HoRyu NariJeong HyunjinSong Young-DoSeo Kyoung YulLee SanghyukKim Dae-Won - Osteoarthritis (OA) is a multifactorial joint disease characterized by progressive cartilage degradation, synovial inflammation, and subchondral bone remodeling. Despite its significant global health burden, there are currently no disease-modifying pharmacological therapies for OA. Gene therapy, leveraging viral and non-viral vectors to deliver therapeutic transgenes into the joint environment, shows significant promise. This mini-review highlights recent innovations in OA gene therapy pipelines, focusing on Platforms employing recombinant adenovirus, adeno-associated virus (AAV), and herpes simplex virus vectors. Strategies include AAV-mediated delivery of interleukin-1 receptor antagonist (IL-1Ra) and truncated nkx3.2 transcription factor to modulate inflammation and promote chondrocyte survival. Non-viral approaches, such as plasmid DNA encoding interleukin-10, are also under investigation. Emerging data from preclinical and clinical studies demonstrate the feasibility of achieving sustained, intra-articular transgene expression with therapeutic efficacy in animal models and early-phase human trials. However, challenges persist, including immune barriers to repeat dosing, variability in vector performance, and the high costs of treatment. Additionally, agerelated declines in transduction efficiency, the heterogeneity of OA, and systemic metabolic influences complicate therapeutic outcomes. To overcome current regulatory obstacles, future research must prioritize the refinement of vector systems to enhance safety, potency, and specificity, as well as the development of combination therapies integrating genetic and conventional approaches, targeting pain and improving function. Gene therapy has transformative potential for improving OA management and an important priority is multidisciplinary collaboration to translate preclinical innovations into accessible, effective treatments for a highly heterogeneous and aging patient population. - Source: PubMed
Publication date: 2025/07/04
Peitso ValtteriNg KarmanEllis RonReginster Jean-YvesEvans Christopher HMobasheri Ali - NKX3-2, a transcriptional repressor factor belonging to the NK family of homeobox-containing proteins, has been widely studied for its role in promoting chondrogenic differentiation and homeostasis. NKX3-2 is upregulated in chemoresistant ovarian tumors and metastatic gastric cancer cells; however, its prognostic role and mechanistic involvement in cancer cell biology remain to be elucidated. By interrogating the TCGA database, we found that cancer patients with high - expression had a shorter overall survival rate than patients with low expression. In ovarian cancer patients, NKX3-2 negatively correlates with P53. Given the prominent role of the latter oncosuppressor in controlling DNA repair and cell death, here we investigate the molecular mechanism involved in this negative correlation in several ovarian cancer cell lines expressing different levels of the two proteins. We found that the high expression of endogenous or ectopic P53 reduced NKX3-2 protein expression, while its knockdown increased it. In contrast, the genetic manipulation of NKX3-2 expression did not affect P53 expression. Mechanistically, P53-mediated downregulation of NKX3-2 does not entail transcriptional activity or proteasomal clearance but occurs via P53-NKX3-2 protein-protein interaction, which in turn results in P53-induced NKX3-2 degradation via the autophagy-lysosome pathway. Remarkably, patients bearing a tumor characterized by low and high expression (indicative of active autophagy) display a better prognosis. Taken together, our data indicate that NKX3-2 represents a negative prognostic factor under P53 control in ovarian cancer. From a translational point of view, identifying this novel mechanism may represent a new molecular signature capable of predicting the clinical outcome of patients, a crucial aspect of developing personalized therapeutic approaches. - Source: PubMed
Publication date: 2025/05/22
Ferraresi AlessandraGhezzi IanSalwa AmreenLualdi ChiaraDhanasekaran Danny NIsidoro Ciro - Marine mammals provide a valuable model for studying the molecular basis of convergent evolution during secondary aquatic adaptation. Using multi-omics data and functional experiments, including CRISPR-Cas9 mouse models and luciferase reporter assays, this study explored the molecular mechanisms driving this transition across coding regions, regulatory elements, and genomic architecture. Convergent amino acid substitutions in and were found to promote lipid accumulation and suppress cancer cell proliferation, likely contributing to the evolution of extensive blubber layers and cancer resistance. Convergently evolved conserved non-exonic elements (CNEs) and lineage-specific regulatory variations were shown to influence the activity of nearby genes (e.g., , , ), shaping cetacean limb phenotypes. Additionally, convergent shifts in topologically associating domains (TADs) across cetaceans and pinnipeds were implicated in the regulation of and expression, playing a role in the formation of thickened blubber layers and mitigating cancer susceptibility. Structural variations within conserved TADs were associated with the expression of neuronal genes, including and , potentially driving cognitive and social adaptations. These findings provide novel insights into the molecular foundations of the convergent evolution of secondary aquatic adaptations in mammals. - Source: PubMed
Publication date: 2025/01/03
Xu ShixiaShan LeiTian RanYu ZhenpengSun DiZhang ZhenhuaSeim IngeZhou MingSun LinxiaLiang NaZhang QianChai SiminYin DaiqingDeme LuoyingWu TianzhenChen YongjieXu ZhikangZheng YuRen WenhuaYang Guang