FGFR3 ELISA Kit (DEIA-XYA659)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
cultured cells
Species Reactivity
Human, Mouse, Rat
Intended Use
The FGFR3 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor FGFR3 protein expression profile in cells. The kit can be used for measuring the relative amounts of FGFR3 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on FGFR3.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 1 plate
2. 10x TBS: 24 mL (10x), Clear
3. Quenching Buffer: 24 mL (1x), Clear
4. Blocking Buffer: 50 mL (1x), Clear
5. 10x Wash Buffer: 50 mL (10x), Clear
6. 100x Anti-FGFR3 Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
8. HRP-Conjugated Anti-Rabbit IgG Antibody: 6 mL (1x), Glass
9. HRP-Conjugated Anti-Mouse IgG Antibody: 6 mL (1x), Glass
10. Primary Antibody Diluent: 12 mL (1x), Clear
11. Ready-to-Use Substrate: 12 mL (1x), Brown
12. Stop Solution: 12 mL (1x), Clear
13. Crystal Violet Solution: 6 mL (1x), Glass
14. SDS Solution: 24 mL (1x), Clear
15. Adhesive Plate Seals: 4 seals
Storage
4°C/6 Months

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References


Molecular characterization of low grade and high grade bladder cancer

PLOS ONE

Authors: Apollo, Alessandro; Ortenzi, Valerio; Scatena, Cristian; Zavaglia, Katia; Aretini, Paolo; Lessi, Francesca; Franceschi, Sara; Tomei, Sara; Sepich, Carlo Alberto; Viacava, Paolo; Mazzanti, Chiara Maria; Naccarato, Antonio Giuseppe

Background Bladder cancer (BC) is the 9th most common cancer diagnosis worldwide. Low grade (LG) represents 70% of all BCs, characterized by recurrence and rare ability (10-15%) to progress to high grade (HG) and invade. The remaining 30% is high grade (HG), fast invasive BC, which is resistant to therapy. Identifying biomarkers for predicting those tumors able to progress is a key goal for patient outcome improvement. This study focuses on the most promising prognostic markers. Materials and methods TP53 and FGFR3 mutational status, Survivin, CK19, CK20, E-cadherin and CD44 gene expression analysis were performed on 66 BCs. Results Survivin was found associated to tumor grade (p<0.05). Moreover, Survivin correlated with CD44 in TP53 wild type (p = 0.0242) and FGFR3 wild type (p = 0.0036) tumors. In particular the Survivin-CD44 correlation was associated to HG FGFR3 wild type BCs (p = 0.0045). Unsupervised hierarchical clustering based on gene expression data identified four distinct molecular groups reflecting the patient histology (p = 0.038). Conclusion We suggest Survivin, both as a biomarker associated to G3 BCs but negatively related to TP53 mutational status, and as a potential novel therapeutic target.

Identification of microRNA transcriptome reveals that miR-100 is involved in the renewal of porcine intestinal epithelial cells

SCIENCE CHINA-LIFE SCIENCES

Authors: Zou, Lijun; Xiong, Xia; Yang, Huansheng; Wang, Kexing; Zhou, Jian; Lv, Dinghong; Yin, Yulong

MicroRNAs play important roles in various cellular processes, including differentiation, proliferation and survival. Using a pig model, this study sought to identify the miRNAs responsible for crypt-villus axis renewal of the small intestinal epithelium. Compared to the villus upper cells, there were 15 up-regulated and 41 down-regulated miRNAs in the crypt cells of the jejunum. Notably, we found that miR-100 was expressed more in the villus upper cells than in the crypt cells, suggesting an effect on intestinal epithelium differentiation. Overexpression of miR-100 increased the activity of alkaline phosphatase, confirming that miR-100 promoted IPEC-J2 cell differentiation. MiR-100 can inhibit cell proliferation as evidenced by CCK-8 and cell cycle assay results. We also showed that miR-100 significantly inhibited the migration of IPEC-J2 cells and promoted cell apoptosis through caspase-3-dependent cleavage of Bcl-2. Furthermore, FGFR3 was identified as a potential target of miR-100 by bioinformatics analysis. We confirmed that overexpression of miR-100 suppressed FGFR3 expression in IPEC-J2 cells by directly targeting the FGFR3 3-UTR. This is the first report of miRNAs acting on the renewal of the intestinal crypt-villus axis. Our results also showed that miR-100 promotes the differentiation and apoptosis, and inhibits the proliferation and migration of enterocytes of pigs.

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