Prox1 EMSA Kit Prospero homeobox protein 1
- Known as:
- Prox1 EMSA Kit Prospero homeobox protein 1
- Catalog number:
- GS-0056
- Product Quantity:
- 30
- Category:
- -
- Supplier:
- Signosis 2011
- Gene target:
- Prox1 EMSA Kit Prospero homeobox protein 1
Related genes to: Prox1 EMSA Kit Prospero homeobox protein 1
- Gene:
- PROX1 NIH gene
- Name:
- prospero homeobox 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-18
- Date modifiied:
- 2016-10-05
Related products to: Prox1 EMSA Kit Prospero homeobox protein 1
Related articles to: Prox1 EMSA Kit Prospero homeobox protein 1
- Lipedema and obesity are often misdiagnosed or clinically confused yet arise via distinct mechanisms, complicating diagnosis and treatment. This review synthesizes evidence differentiating these conditions across genetic, hormonal, inflammatory and mechanical pathways to identify therapeutic targets. Lipedema may involve genetic predisposition (forkhead box C2 [FOXC2], prospero homeobox 1 [PROX1]), hormonal dysregulation with aberrant aromatase activity, and altered adipogenesis (peroxisome proliferator-activated receptor gamma [PPARγ], CCAAT/enhancer-binding protein [C/EBP]). A proinflammatory microenvironment with macrophage M1/M2 imbalance, elevated interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and extracellular matrix remodeling is hypothesized to drive fibrosis. Emerging evidence implicates gut-derived endotoxemia (lipopolysaccharide [LPS]-toll-like receptor 4 [TLR4]-nuclear factor kappa-B [NF-κB]) and mechanotransduction (Yes-associated protein [YAP]/transcriptional coactivator with PDZ-binding motif [TAZ]) in adipocyte hypertrophy and treatment resistance. Obesity involves systemic metabolic dysfunction with visceral adiposity and cardiometabolic comorbidities. Lipedema patients maintain metabolic health, exhibit gluteofemoral fat distribution and experience neuropathic pain via nociceptor sensitization (transient receptor potential vanilloid 1 [TRPV1] and ankyrin 1 [TRPA1]) with central amplification. Weight-loss interventions are ineffective, necessitating targeted strategies. Promising targets include TLR4 antagonism, vascular endothelial growth factor C/vascular endothelial growth factor receptor-3 (VEGF-C/VEGFR3) modulation for lymphatic enhancement, YAP/TAZ inhibition and neuromodulators for pain. Physical therapy functions as a biological modifier targeting inflammation, lymphatic drainage and mechanotransduction. This review highlights promising but largely hypothesis-generating molecular insights and calls for validated biomarkers, rigorous clinical trials, and mechanism-based therapies. Many of the pathways discussed require further confirmation in human studies. - Source: PubMed
Publication date: 2026/09/01
Güney Yiğit EgeDemiralay Sıla ÇağlaKeser İlke - The association between lymphovascular invasion (LVI) and outcomes in dogs with thyroid carcinoma is inadequately described, and a standardized definition of LVI is lacking. This study's objectives were to histopathologically and immunohistochemically characterize LVI and to evaluate associated clinical outcomes in dogs with thyroid carcinoma. Inclusion criteria were: dogs that underwent thyroidectomy for thyroid carcinoma with available histopathology samples, and a minimum of 1-year postoperative follow-up data or follow-up to death. Thirty dogs with 35 distinct tumours, including 26 follicular and nine medullary, were evaluated. LVI was characterized as intracapsular endothelialized tumour emboli (without adhered fibrin) in 26 samples, intracapsular tumour emboli with adhered fibrin in seven samples, extracapsular tumour emboli without adhered fibrin in 10 samples, and extracapsular tumour emboli with endothelial disruptions and adhered fibrin in three samples. CD31 and Prox1 positive vessels contained endothelialized tumour thrombi in 17 and one sample, respectively. Extracapsular invasion with (non-endothelialized) and without (endothelialized) associated fibrin were associated with a 10-fold (p = 0.001) and 3-fold (p = 0.013) increase in the likelihood of death, respectively. No significant difference in the likelihood of death was noted between cases of extracapsular invasion with or without fibrin (p = 0.31). Intracapsular tumour thrombi with or without associated fibrin and non-endothelialized tumour thrombi were not associated with outcomes in this cohort. These results support that in dogs with thyroid carcinoma, extracapsular LVI with or without associated fibrin thrombi, but not intracapsular LVI, is associated with worse outcomes. Further study is warranted on a larger population of dogs with standardized treatment and follow-up. - Source: PubMed
Publication date: 2026/09/24
Griffin Maureen AStoyle BriannaOakes AllieFlesner BrianLenz Jennifer AStefanovski DarkoDurham Amy C - Metabolic dysfunction-associated steatohepatitis (MASH) represents a major global health burden, bridging isolated steatosis, progressive fibrosis and hepatocellular carcinoma. Recent paradigms highlight ferroptosis, an iron-dependent, lipid-peroxidation-driven form of regulated cell death, as a primary lytic initiating event in metabolic liver injury. In this review, we delineate the ferroptosis-immune axis in MASH, characterising it as a self-amplifying, bidirectional circuit. In this framework, parenchymal ferroptotic rupture and damage-associated molecular pattern emission drive myeloid activation and pro-inflammatory cytokine release. This inflammatory microenvironment reciprocally triggers cell-autonomous Kupffer cell ferroptosis and homeostatic collapse. We establish a novel cell-type-specific transcriptomic framework governed by a core four-gene signature (, , and ) that maps the transition from early metabolic stress to advanced structural remodelling. Furthermore, we decode the substrate paradox of polyunsaturated fatty acids, illustrating how their role shifts from physiological signalling to executioner substrates when antioxidant systems collapse. This biophysical vulnerability is heavily primed by inherited gene polymorphisms, including , and By evaluating the sexual dimorphism embedded within these pathways, specifically how the DTL-PROX1 axis dictates distinct iron accumulation rates and lipid peroxidation sensitivities, we propose precise clinical stratification strategies. Finally, we outline actionable translational avenues, highlighting how targeting the ferroptosis-immune axis offers a highly specific therapeutic window to arrest lipotoxicity, suppress inflammation and disrupt oncogenic priming before irreversible tissue remodelling occurs. - Source: PubMed
Publication date: 2026/09/10
Kuchay Mohammad ShafiCubero Francisco JavierRamos-Molina Bruno - The engineering of a 3D lymphatic collecting vessel has been of recent interest due to the lack of treatments for lymphatic valve disruptions. While oscillatory shear stress has been shown to regulate lymphatic collecting vessel morphogenesis, its effect in the context of physiologically relevant extracellular matrix remains elusive. In this study, we used a microfluidic device to elucidate the effect of oscillatory shear stress on human lymphatic endothelial cells cultured on dopamine-modified hyaluronic acid or fibronectin. Here, we show that hyaluronic acid can synergistically enhance mechanoresponsive morphological changes, activate cytoskeleton localization, induce nuclear expression of key mechanosensitive markers (PROX1 and FOXC2), amplify mechanotransduction pathways (VE-CAD and mTORC1), and downregulate capillary lymphatic markers (PDPN and LYVE-1). These results highlight the potential of hyaluronic acid-based materials for the generation of 2D and 3D lymphatic collecting vessel models. - Source: PubMed
Publication date: 2026/09/04
Lightsey N KeilanyFluskey GraceCruz-Gonzalez BrendaFan FeiSaha SanjoyHall EvaHanjaya-Putra Donny - Lymphatic vessels play essential roles in maintaining fluid homeostasis and responding to inflammatory and tissue environmental changes. During these biological processes, lymphatic endothelial cells (LECs) lining lymphatic vessels adapt to external stimuli in various organs and alter their characteristics. While organ-specific molecular and functional heterogeneity has been well-characterized in blood vascular endothelial cells, the extent and functional significance of such heterogeneity in LECs remain poorly understood. In this study, we established LECs derived from the heart and lung tissues of Prox1-GFP mice for comparative analyses. Both cell types retained lymphatic endothelial marker expression and exhibited tube-forming capacity in two- and three-dimensional culture systems, indicating the preservation of functional LEC phenotypes. Transcriptomic analysis revealed that LEC gene expression profiles were primarily segregated according to the organ of origin, indicating that LECs possess stable organ-specific transcriptional states. Notably, cardiac-derived LECs displayed enrichment of proliferation-related pathways, including MYC signaling, as well as inflammatory pathways such as TNF-α-NFκB and IL2-STAT5 signaling, indicating a transcriptional state primed for enhanced responsiveness to external stimuli. Furthermore, cardiac-derived LECs exhibited increased susceptibility to TGF-β-induced endothelial-to-mesenchymal transition (EndoMT) compared with pulmonary-derived LECs, reflecting enhanced cellular plasticity. These findings demonstrate that organ-specific transcriptional states regulate stimulus responsiveness, thereby defining cellular plasticity in LECs. - Source: PubMed
Publication date: 2026/07/20
Tsuyama YujiTakahashi KazukiKobayashi MihoBenzemam Suzuki LucasAkagi HarukaYokozawa MikiImafuku TadashiHashimoto ShinichiMatsunaga YukikoItoh FumikoHarada HiroyukiHong Young-KwonWatabe Tetsuro