Rap2A antibody (FITC)
- Known as:
- Rap2A (anti-) (fluorecein)
- Catalog number:
- orb7611
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Rap2A antibody (FITC)
Related genes to: Rap2A antibody (FITC)
- Gene:
- RAP2A NIH gene
- Name:
- RAP2A, member of RAS oncogene family
- Previous symbol:
- RAP2
- Synonyms:
- K-REV
- Chromosome:
- 13q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
Related products to: Rap2A antibody (FITC)
Related articles to: Rap2A antibody (FITC)
- Alzheimer's disease (AD) is a common neurodegenerative disorder in the elderly population, and early screening can effectively delay the progression of the disease. Mild cognitive impairment (MCI) occurs prior to the onset of AD; however, the accuracy of existing MCI-to-AD prediction methods remains relatively low. Additionally, small sample sizes and high feature dimensions often lead to model overfitting, highlighting the need for effective early screening approaches. To address the aforementioned issues, this study integrated non-paired multi-modal features-including clinical indicators from the ADNI database, blood biomarkers, brain region volume features extracted from MRI, and genetic biomarkers from the GEO database-and proposed a gender-corrected random matching strategy. The Random Forest algorithm was adopted to evaluate this strategy, analyze feature importance, and compare the performance of 9 machine learning algorithms based on the top 40 ranked features. The predictive performance of multi-modal data was superior to that of single-modal data, and the proposed strategy achieved favorable results in early AD screening. 16 specific genetic features (e.g., IFI27, EDF1, RAP2A, KIF5C, SERPINA3, FBXW7, IFITM1, ISG15, PSMB3, APOE4, KCNB1, PSPH, HMGN2, S100A13, IFIT3, and CALM1) and 6 brain region volume features ranked high in terms of importance. When validated using paired datasets from ADNI across the 9 algorithms, ensemble learning models demonstrated significantly stronger fitting capabilities. The non-paired multi-modal fusion approach not only expands the sample size but also enhances the generalization ability and robustness of the model. This provides a theoretical basis for the application of this strategy in the field of small-sample medical research. - Source: PubMed
Publication date: 2026/03/06
Zhang ZhihaoZhang RuixiaYang WenzhongLv KeWu MiaoXu Lianghui - The current study assesses the efficacy of Pediococcus acidilactici (PA) as a water-added probiotic in Pacific white shrimp (Litopenaeus vannamei), evaluating its impact on water quality, growth, feed efficiency, body composition, digestive enzymes, immune response, tissue structure, gene expression, and disease resistance. A 10-week experiment was conducted to assess these effects. Shrimp, each with an initial weight of 4.3 ± 0.07 g, were divided into four groups: a control group (without probiotic water addition) and three treatment groups receiving PA at 0.1 g/m (G1), 0.2 g/m (G2), and 0.3 g/m (G3). The shrimp (n = 600) were randomly distributed into twelve concrete ponds (50 shrimp per pond). Results indicated a significant decrease in water ammonia and total ammonia nitrogen concentrations following P. acidilactici supplementation (P<0.001). Notably, only groups G2 and G3 significantly decreased pH compared to the other experimental groups (P < 0.001). Final weight, weight gain, weight gain percentage, average daily gain, and specific growth rate were significantly improved by the P. acidilactici water additive in a dose-dependent manner (P < 0.001). Both survival rate and final shrimp number were significantly improved in all P. acidilactici water additive groups compared to control groups (P < 0.001). Furthermore, the feed conversion ratio and lipid peroxidation significantly decreased in all P. acidilactici-supplemented groups. The addition of PA to the water led to an increase in ash content and a significant decrease in crude lipid and moisture (P < 0.01) in shrimp carcasses. Digestive enzymes (amylase, lipase, and protease), immunological variables (total haemocyte count, lysozyme activity, and phenoloxidase), and antioxidant enzymes (CAT, SOD, and GPx) were significantly higher in all P. acidilactici-supplemented groups (P < 0.001) compared to the control group. Molecular analysis indicated higher expression of growth-related genes (IGF-II and Rap-2a), immune genes (lectin and penaeidin), and antioxidant-related genes (CAT and GPX) in shrimp receiving higher PA doses (P < 0.001). Microscopic examination showed that the water PA-additive group had well-organized hepatopancreatic tubules, which were distinguishable by diverse epithelial cells rich in secretory vesicles compared to the non-additive group. The water-based administration of the P. acidilactici (PA) additive also significantly enhanced the shrimp's resistance to Vibrio parahaemolyticus. Collectively, these findings suggest that PA supplementation at 0.3 g/m3 optimizes growth performance, survival rates, and holistic shrimp health, offering a sustainable alternative for disease management in aquaculture. - Source: PubMed
Publication date: 2026/02/13
Said Radwa MHendam Basma MAbd Al-Kareem Omayma MMahmoud Nehad M SOsailan RahaYounis Nehal AMansour Yasmine AAly Mohamed Y MEl Araby Rania El Sayed - Idiopathic pulmonary fibrosis (IPF) is characterized by progressive fibrotic remodeling accompanied by persistent endothelial activation and leukocyte infiltration. Although endothelial dysfunction is increasingly recognized as a key contributor to fibrogenesis, the intracellular signaling pathways that couple inflammatory cues to endothelial-immune interactions remain incompletely defined. Ras-related protein Rap2a (RAP2A), a small GTPase implicated in stress and inflammatory signaling, has not been systematically investigated in pulmonary endothelial cells during fibrotic lung injury. Here, using a bleomycin-induced experimental lung fibrosis model, we observed that RAP2A expression was markedly upregulated in pulmonary endothelial cells and correlated with disease severity. Endothelium-enriched knockdown of Rap2a via AAV9-Cdh5-shRNA attenuated inflammatory cell adhesion to the pulmonary endothelium, reduced fibrotic remodeling, and improved lung function. Mechanistically, RAP2A promoted endothelial activation by enhancing MAP4K4-dependent signaling and upregulating vascular cell adhesion molecule 1 (VCAM1) in response to pro-inflammatory stimulation, thereby facilitating leukocyte-endothelial interactions. In vitro assays further demonstrated that RAP2A deficiency impaired tumor necrosis factor-α-induced endothelial adhesiveness without affecting basal endothelial integrity. Collectively, our findings identify endothelial RAP2A as a regulator of inflammatory endothelial activation in experimental lung fibrosis and suggest that targeting RAP2A-mediated signaling may represent a potential strategy to modulate endothelial-immune crosstalk during fibrotic lung injury. - Source: PubMed
Publication date: 2026/02/11
Zheng XiaolanYue PengZhou KaiyuGong GuidongZhang YueLin ShaLiu XuZheng YanjiangJing SiyuanGuo JunlingQi YanDing Bi-SenHua YiminLi Yifei - Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the TUNEL assay experiments shown in Fig. 2E on p. 5, the Merge panels for the shFLVCR1‑AS1 experiments shown for the Caco‑2 and SW480 cell lines appeared to have been inserted into this figure the wrong way around. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 23: 139, 2021; DOI: 10.3892/mmr.2020.11778]. - Source: PubMed
Publication date: 2025/12/12
Han YiWang XiaoyanMao EnqiangShen BoyongHuang Liang - Asymmetric cell division (ACD) is a fundamental process to balance cell proliferation and differentiation during development and in the adult. Cancer stem cells (CSCs), a very small but highly malignant population within many human tumors, are able to provide differentiated progeny by ACD that contribute to the intratumoral heterogeneity, as well as to proliferate without control by symmetric, self-renewing divisions. Thus, ACD dysregulation in CSCs could trigger cancer progression. Here, we consistently find low expression levels of , the human homolog of the ACD regulator , in glioblastoma (GBM) patient samples, and observe that scarce levels of are associated with poor clinical prognosis in GBM. Additionally, we show that restitution of RAP2A in GBM neurosphere cultures increases the ACD of glioblastoma stem cells (GSCs), decreasing their proliferation and expression of stem cell markers. Our results support that ACD failures in GSCs increase their spread and ACD amendment could contribute to reduce the expansion of GBM. - Source: PubMed
Publication date: 2025/11/28
Franco MaribelGargini RicardoBarberá Víctor MBecerra DanielSaceda MiguelCarmena Ana