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)
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Related articles to: NKX3-2 antibody - middle region (ARP33200_P050)
- The BMP7-derived peptide p[63-82] improves a healthy chondrocyte phenotype and attenuates chondrocyte hypertrophy in human osteoarthritic chondrocytes. In cartilage regeneration strategies, chondrogenic differentiation of progenitor cells is often hampered by hypertrophic differentiation of the newly formed cartilaginous tissue. In this study, we explored the pro-chondrogenic and anti-hypertrophic effects of peptide p[63-82] in different progenitor-based chondrogenic differentiation models. Chondrogenic differentiation was induced in ATDC5 cells, human bone marrow-derived stem cells (hBMSCs), and rabbit periosteal progenitor cells (rPCs) in the absence or presence of peptide p[63-82]. In all models, increased gene expression of Sox9, Nkx3.2, Col2a1, Acan and GAG content was observed in the peptide p[63-82] condition, indicative of a pro-chondrogenic effect. Expression of hypertrophic genes Runx2, Col10a1, Alpl and Rmrp and ALP enzyme activity were prevented by the p[63-82] peptide-exposed cultures. Nkx3.2 signaling is, partly, responsible for the observed p[63-82] effects. The peptide p[63-82] was thus able to promote a chondrogenic phenotype, whilst preventing the development of chondrocyte hypertrophy in ATDC5 cells, hBMSCs and rPCs. The p[63-82] peptide could be a promising candidate for optimizing cell-based cartilage repair strategies after validation in in vivo models. - Source: PubMed
Publication date: 2026/09/23
Zhang MingzhengPeeters Laura C WEmans Pieter JWitlox Adhiambo M Avan den Akker Guus G HWelting Tim J MCaron Marjolein M J - Cone-rod dystrophy (CRD) is an inherited retinal dystrophy characterized by decreased visual acuity, color vision defects, and progressive loss of peripheral vision. RAB28-associated CRD is genetically homogeneous and results from pathogenic variants in the RAB28 gene, which is essential for photoreceptor function. - Source: PubMed
Publication date: 2026/06/03
Park JoonhongJang WooriAhn YoojungLee Haeng-Jin - 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