Cat.No. : AD00134Z
Titer: ≥1x10^10 IFU/mL / ≥1x10^11 IFU/mL / ≥1x10^11 VP/mL / ≥1x10^12 VP/mL Size: 100 ul/500 ul/1 mL
Storage: -80℃ Shipping: Frozen on dry ice
| Cat. No. | AD00134Z |
| Target Gene | CAMKK2 |
| Product Type | Adenoviral particle |
| Insert | CAMKK2 |
| Titer | Varies lot by lot, for example, ≥1x10^10 IFU/mL, ≥1x10^11 IFU/mL, ≥1x10^11 VP/mL etc. |
| Size | Varies lot by lot, for example, 250 ul, 500 ul, 1 mL etc. |
| Storage | Store at -80℃. Avoid multiple freeze/thaw cycles. |
| Shipping | Frozen on dry ice |
| Creative Biogene ensures high-quality adenovirus particles by optimizing and standardizing production protocols and performing stringent quality control (QC). The specific QC experiments performed vary between adenovirus particle lots. | |
| Endotoxin | Endotoxins, primarily derived from Gram-negative bacteria, can trigger adverse immune responses. Endotoxin contamination is a significant concern in adenovirus production, especially for applications in animal studies and gene therapy. Creative Biogene utilizes rigorous endotoxin detection methods to monitor the endotoxin level in our produced adenovirus particles to ensure regulatory compliance. |
| Sterility | Creative Biogene ensures that adenovirus products are free of any bacterial, fungal and other microbial contamination. |
| Ad5 E1 Detection | All Creative Biogene adenoviruses are PCR tested to ensure that there are no detectable E1 sequences in the particles, which could be from revertants or external E1 contamination. |
| RCA Assays | Adenovirus products originating at Creative Biogene are guaranteed to have undetectable replication-competent adenovirus (RCA). This quality control measure is important because there is always the possibility of wild-type contamination due to revertants or environmental sources. |
| PFU Titering | All purified adenovirus preparations are tested for infectious titer. Creative Biogene's PFU test takes a few days longer but counts true plaques in HEK cells rather than estimating PFU titers via IHC staining or TCI50 of infected cells. |
Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) regulates a variety of biological processes and is implicated in a variety of pathological processes. However, its role in myocardial ischemia/reperfusion (MI/R) injury remains unknown. Here, researchers show that MI/R in vivo or hypoxia/reoxygenation (H/R) in vitro induces a decrease in CaMKK2 levels. Upregulation of CaMKK2 in rats ameliorates MI/R-induced cardiac damage, while suppressing cardiac cell apoptosis, oxidative stress, and proinflammatory responses. CaMKK2-overexpressing rat cardiomyocytes are also protected from H/R injury by suppressing apoptosis, oxidative stress, and proinflammatory responses. CaMKK2 overexpression leads to increased AMPK, AKT, and GSK-3β phosphorylation and enhances Nrf2 activation under MI/R or H/R conditions. AMPK inhibition abolishes CaMKK2-mediated Nrf2 activation and the associated cardioprotective effects. Inhibition of Nrf2 also attenuated the associated cardioprotective effects mediated by CaMKK2. Thus, upregulation of CaMKK2 enhances the Nrf2 pathway through regulating AMPK/AKT/GSK-3β, thereby providing therapeutic benefits in a rat model of MI/R injury, suggesting that CaMKK2 is a novel molecular target for the treatment of MI/R injury.
The researchers investigated the effect of CaMKK2 overexpression on H/R injury in vitro. CaMKK2 was overexpressed in cardiomyocytes using a recombinant adenovirus carrying CAMKK2 (Ad-CaMKK2). Ad-CaMKK2 infection resulted in increased CaMKK2 levels in cultured cardiomyocytes (Figure 1A, B). CCK-8 assays showed that upregulation of CaMKK2 attenuated the deleterious effects of H/R on cell viability (Figure 1C). H/R led to a significant increase in apoptosis, which was reduced in CaMKK2-overexpressing cardiomyocytes (Figure 1D, E). The increased Bax levels and decreased Bcl2 levels caused by H/R were reversed by CaMKK2 overexpression (Figure 1F). In addition, overexpression of CaMKK2 also attenuated the H/R-induced overproduction of ROS (Figure 1G) and proinflammatory mediators in cultured cardiomyocytes.
Figure 1. The effect of CaMKK2 up-regulation on H/R injury. Cardiomyocytes were infected with Ad-CaMKK2 for 72 h before H/R injury. (Li C, et al., 2023)
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The virus showed excellent transduction efficiency in our experiments, and the customer service team was responsive when I had questions. Shipping was fast, and the packaging ensured the product arrived intact. Highly recommend!
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