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

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nuclear, cell lysates
Species Reactivity
Human, Mouse, Rat
Contents of Kit
1. 12x 8-Well dsDNA Oligonucleotide Coated Microstrips
2. 100x Anti-Phospho Target Primary Antibody
3. 100x Anti-Target Primary Antibody
4. HRP-Conjugated Anti-Rabbit IgG Secondary Antibody
5. Nuclear Lysate Positive Control
6. Wild-Type Consensus dsDNA Oligonucleotide
7. Mutant Consensus dsDNA Oligonucleotide
8. 10x Wash Buffer
9. 2x Binding Buffer
10. Primary Antibody Diluent
11. 100x Protease and Phosphatase Inhibitors
12. Nuclear Wash Buffer
13. Cytoplasmic Extraction Buffer
14. Nuclear Extraction Buffer
15. Ready-to-Use Substrate
16. Stop Solution
17. Adhesive Plate Seals
18. Technical Manual
4°C/6 Months


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The regulation of Akt and FoxO transcription factors during dehydration in the African clawed frog (Xenopus laevis)


Authors: Luu, Bryan E.; Zhang, Yichi; Storey, Kenneth B.

The African clawed frog (Xenopus laevis) naturally tolerates severe dehydration using biochemical adaptation, one of which is the elevation of antioxidant defenses during whole-body dehydration. The present study investigated the role and regulation of a pathway known to regulate oxidative stress response, the Akt-FoxO signaling pathway, in clawed frog skeletal muscle, responding to medium (15%) and high (30%) dehydration. Protein levels of total and phosphorylated Akt, FoxO1, and FoxO3 were assessed via immunoblotting, in addition to the levels of the E3 ubiquitin ligase known to be associated with muscle atrophy, MAFbx. Akt activity/phosphorylation in addition to its total protein levels were decreased in the skeletal muscle during dehydration, and this corresponded with decreases in the relative phosphorylation of FoxO1 and FoxO3 as well on several residues. Akt is an inhibitor of FoxO1 and FoxO3 activity via phosphorylation, suggesting that FoxO activities were increased during dehydration stress. Furthermore, MAFbx showed decreased protein expression during high dehydration as well, suggesting that the clawed frog may exhibit some natural resistance to skeletal muscle atrophy during severe dehydration conditions. In addition to identifying that the suppression of Akt could lead to an activation of FoxO transcription factors in X. laevis during dehydration, these investigations suggest that X. laevis dehydration may implicate FoxO1 and FoxO3 in controlling skeletal muscle atrophy in X. laevis exposed to dehydration. This study implicates the Akt signaling pathway, its regulation of FoxO transcription factors, and FoxO-controlled targets, in stress adaptation against dehydration.

Effective Delivery of Hypertrophic miRNA Inhibitor by Cholesterol-Containing Nanocarriers for Preventing Pressure Overload Induced Cardiac Hypertrophy


Authors: Zhi, Ying; Xu, Chen; Sui, Dandan; Du, Jie; Xu, Fu-Jian; Li, Yulin

Persistent cardiac hypertrophy causes heart failure and sudden death. Gene therapy is a promising intervention for this disease, but is limited by the lack of effective delivery systems. Herein, it is reported that CHO-PGEA (cholesterol (CHO)-terminated ethanolamine-aminated poly(glycidyl methacrylate)) can efficiently condense small RNAs into nanosystems for preventing cardiac hypertrophy. CHO-PGEA contains two features: 1) lipophilic cholesterol groups enhance transfection efficiency in cardiomyocytes, 2) abundant hydrophilic hydroxyl groups benefit biocompatibility. miR-182, which is known to down-regulate forkhead box O3, is selected as an intervention target and can be blocked by synthetic small RNA inhibitor of miR-182 (miR-182-in). CHO-PGEA can efficiently deliver miR-182-in into hearts. In the mice with aortic coarctation, CHO-PEGA/miR-182-in significantly suppresses cardiac hypertrophy without organ injury. This work demonstrates that CHO-PGEA/miRNA nanosystems are very promising for RNA-based therapeutics to treat heart diseases.

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