Cat.No. : AD00172Z
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. | AD00172Z |
| Target Gene | FTO |
| Product Type | Adenoviral particle |
| Insert | FTO |
| 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. |
| Gene Name | FTO fat mass and obesity associated [ Homo sapiens ] |
| Gene Symbol | FTO |
| Synonyms | FTO; fat mass and obesity associated; alpha-ketoglutarate-dependent dioxygenase FTO; KIAA1752; MGC5149; protein fto; fat mass and obesity-associated protein; |
| Gene ID | 79068 |
| UniProt ID | Q9C0B1 |
| mRNA Refseq | BC003583 |
| Chromosome Location | 16q12.2 |
| Function | DNA-N1-methyladenine dioxygenase activity; ferrous iron binding; metal ion binding; oxidative DNA demethylase activity; oxidative RNA demethylase activity; oxidoreductase activity, acting on single donors with incorporation of molecular oxygen, incorporation of two atoms of oxygen; |
| MIM | 610966 |
Activation of hepatic stellate cells (HSCs) is central to the development of liver fibrosis. Autophagy promotes HSC activation and ultimately accelerates liver fibrosis. Unc-51-like autophagy-activating kinase 1 (ULK1) is a mammalian autophagy promoter, and N6-methyladenosine (m6A) modification is closely associated with autophagy. In this study, researchers found that the m6A demethylase fat mass and obesity-associated protein (FTO) was the most differentially expressed m6A methylase, which was upregulated during HSC activation and bile duct ligation (BDL)-induced liver fibrosis. Importantly, FTO overexpression exacerbated HSC activation and liver fibrosis through autophagy. Mechanistically, ULK1 is a target of FTO compared with other autophagy-related genes, because FTO primarily mediates m6A demethylation of ULK1 and upregulates its expression, thereby enhancing autophagy and HSC activation. Notably, the m6A reader YTH domain-containing protein 2 (YTHDC2) reduced ULK1 mRNA levels by recognizing m6A binding sites, ultimately inhibiting autophagy and HSC activation. Taken together, these findings highlight that m6A-dependent ULK1 is an important regulator of HSC autophagy and suggest that ULK1 is a new potential therapeutic target for the treatment of liver fibrosis.
To verify the role of FTO in hepatic fibrosis in vivo, the researchers first transfected recombinant adenoviral vector encoding FTO (AdFTO) into mouse livers. HE and Masson staining showed that FTO enhanced inflammatory cell infiltration and collagen deposition in the portal area (Figure 1A). Western blot analysis showed that the expression of α-SMA and type I collagen in the AdFTO group gradually increased (Figure 1C), consistent with the results of immunohistochemical staining (Figure 1B). Previous studies have shown that enhanced autophagy accelerates the occurrence of liver fibrosis. Here, the researchers hypothesized that autophagy is essential for FTO-induced liver fibrosis. To verify this hypothesis, the level of autophagy after FTO treatment was detected. As expected, the conversion of LC3 I to LC3 II in the AdFTO group gradually increased, while the conversion of p62 decreased (Figure 2C), indicating that FTO enhanced autophagy.
Figure 1. FTO promotes HSC activation and hepatic fibrosis as well as autophagy. (Huang T, et al., 2024)
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