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Bio Reagents & Consumables
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- EdU Cell Proliferation Image Kit (Orange Fluorescence)
Cell Detection
EdU Cell Proliferation Image Kit (Orange Fluorescence)
Specifications
| Applications notes | Cell Proliferation EdU Image Kit (Orange Fluorescence) is a novel alternative to the BrdU assay. EdU (5-ethynyl-2´-deoxyuridine) is a nucleoside analog of thymidine and is incorporated into DNA during active DNA synthesis. Comparing to BrdU assays, the EdU-Click Assays are not antibody based and therefore do not require DNA denaturation (typically using HCl or heat or digestion with DNase) for detection of the incorporated nucleoside. Detection is based on a click reaction, a copper-catalyzed covalent reaction between an azide and an alkyne, is complete within 30 minutes. |
Product Properties
| Kit components | • EdU (10mM) •BSA Wash Solution (5×) •AbFluor 545 azide •Reaction buffer (10×) •Copper Reagent •Reducing Agent •Hoechst 33342 (1000×) •Hydroxyurea |
| Features & Benefits | • Optimized negative control is provided to rule out false positives •No antibody needed. • No denaturation steps, preservation of cell morphology and DNA integrity. • Simple, reliable and time-saving than traditional methods. • Proprietary AbFluor 545 azide (Ex/Em = 546/565 nm)-good photostability and minimizing fluorescence quenching. • Optimized for fluorescent microscopy. |
| Storage instructions | Stable for at least 12 months at recommended temperature from date of shipment. Gel pack with blue ice. |
| Shipping | Gel pack with blue ice. |
| Precautions | The product listed herein is for research use only and is not intended for use in human or clinical diagnosis. Suggested applications of our products are not recommendations to use our products in violation of any patent or as a license. We cannot be responsible for patent infringements or other violations that may occur with the use of this product. |
Additional Information
| Background | The detection of cell proliferation is of utmost importance for assessing cell health, determining genotoxicity or evaluating anticancer drugs. Until now, measuring DNA synthesis directly is most accurate method of doing it, normally performed by incorporation of the nucleoside analog like [3H] thymidine or 5-bromo-2’-deoxyuridine to cells during replication, and then detected or visualized by autoradiography or with an anti-BrdU-antibody respectively. |
| Specifications | Kindly refer to the "Overview" tab. |
Author: Cao B, Zhao R, Li H, Xu X, Gao J, Chen L, Wei B.
Publication Name: International Journal of Biological Sciences
IF: 10.75
Everolimus was designed as a mammalian target of rapamycin (mTOR) inhibitor. It has been proven as a targeted drug for gastric cancer (GC) therapy. However, long-term treatment with everolimus may cause severe side effects for recipients. Decreasing the dosage and attenuating the associated risks are feasible to promote clinical translation of everolimus. This study aimed to identify the underlying mechanisms of responses to everolimus and develop novel regimens for GC treatment. Our findings proved that there was a significant dose-dependent relationship of everolimus-induced GC cell apoptosis and glycolysis inhibition. Then, we found that a member of glucose transporter (GLUT12) family, GLUT12, was actively upregulated to counteract the anticancer effects of everolimus. GLUT12 might be overexpressed in GC. High expression of GLUT12 might be correlated with tumor progression and short survival time of GC patients. Bioinformatic analysis suggested that GLUT12 might be involved in regulating cancer development and metabolism. The experiments proved that GLUT12 significantly promoted GC growth, glycolysis and impaired the anticancer effects of everolimus. Androgen receptor (AR) is a classical oncogenic factor in many types of cancer. Everolimus elevated GLUT12 expression in an AR-dependent manner. Inhibition of AR activity abrogated the promotive effects on GLUT12 expression. Both in-vitro and in-vivo experiments demonstrated that GLUT12 knockdown augmented anticancer effects of everolimus. Enzalutamide, an AR inhibitor, or AR knockdown was comparable to GLUT12 suppression. This study identified the role of the AR/GLUT12 pathway in the development of poor responses to everolimus. Interference with AR/GLUT12 pathway may serve as a promising approach to promoting the translational application of everolimus in GC therapy.
Author: Cao B, Deng H, Cui H, Zhao R, Li H, Wei B, Chen L
Publication Name: Cancer Cell Int
IF: 4.175
Correlation and enrichment analyses of PGM1 were conducted based on The Cancer Genome Atlas database. Data derived from the Kaplan–Meier Plotter database were analyzed to evaluate correlations between PGM1 expression and survival time of GC patients. Cell counting kit-8, 5-Ethynyl-2-deoxyuridine, flow cytometry assays, generation of subcutaneous tumor and lung metastasis mouse models were used to determine growth and metastasis in vitro and in vivo. Cell glycolysis was detected by a battery of glycolytic indicators, including lactate, pyruvic acid, ATP production and glucose uptake. Fatty Acid Synthase (FASN) activity and expression levels of lipid enzymes were determined to reflect on lipid metabolism.