Cat.No. : AD00121Z
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. | AD00121Z |
| Target Gene | APLN |
| Product Type | Adenoviral particle |
| Insert | APLN |
| 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. |
Periodontitis is an inflammatory disease of the supporting tissues surrounding teeth, characterized by irreversible destruction of the gingiva, periodontal ligament (PDL), and alveolar bone, leading to tooth loss. Here, researchers elucidated the correlation between periodontitis and apelin (APLN), an adipokine and a regulatory peptide, respectively, which are involved in inflammation and bone remodeling. Moreover, TNF-α treatment downregulated APLN expression in PDL cells and gingival fibroblasts, indicating that APLN has a protective effect against periodontitis progression. Overexpression of APLN or exogenous APLN treatment inhibited TNF-α-mediated MMP1, IL6, and PTGS2 catabolic gene expression in PDL cells. Furthermore, inhibition of the APLNA-PJ axis by the APJ inhibitor ML221 induced catabolic gene expression in PDL cells. Thus, these findings provide evidence for APLN as a regulator of the inflammatory response during periodontitis.
To explore the role of APLN in gingival tissue, the researchers induced APLN overexpression by adenoviral infection of human GFs. In contrast to the results in PDL cells, adenoviral overexpression of APLN in GFs only reduced the mRNA level of PTGS2, but not the mRNA levels of MMP1 and IL6 (Figure 1A). In addition, overexpression of APLN also inhibited the upregulation of PTGS2 expression levels in inflamed GFs treated with IL-1β and TNF-α. However, the expression of MMP1 and IL6 induced by proinflammatory cytokines in GFs was not regulated by APLN overexpression (Figures 1B and 1C). These data suggest that APLN partially inhibits inflammation in gingival tissue during the progression of periodontitis.
Figure 1. Effect of adenoviral APLN overexpression on periodontitis in gingival fibroblasts (GFs). (Lee G, et al., 2019)
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The Human APLN adenoviral particles have been integral to our recent projects. With their high level of specificity and reliable performance, these particles enabled us to make significant progress in our signaling pathway analysis.
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