Cat.No. : AD00185Z
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. | AD00185Z |
| Target Gene | HGF |
| Species | Human |
| Product Type | Adenoviral particle |
| Insert | HGF |
| 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 | HGF hepatocyte growth factor (hepapoietin A; scatter factor) [ Homo sapiens ] |
| Gene Symbol | HGF |
| Synonyms | SF; HGFB; HPTA; F-TCF; DFNB39 |
| Gene Description | hepatocyte growth factor (hepapoietin A; scatter factor) |
| Gene ID | 3082 |
| UniProt ID | P14210 |
| mRNA Refseq | NM_000601.4 |
| Protein Refseq | NP_000592.3 |
| Chromosome Location | 7q21.1 |
| Function | growth factor activity; protein binding; protein heterodimerization activity; NOT serine-type endopeptidase activity; |
| Pathway | Arf6 signaling events, organism-specific biosystem; Cytokine Signaling in Immune system, organism-specific biosystem; Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem; Direct p53 effectors, organism-specific biosystem; FGF signaling pathway, organism-specific biosystem; Focal Adhesion, organism-specific biosystem; |
| MIM | 142409 |
The discovery of c-kit+ cardiac stem cells (CSCs) provides us with a new therapeutic target to repair the damaged heart. Necroptosis is a regulated cell death that has recently been shown to occur after myocardial infarction (MI). Here, researchers investigated the effects of hepatocyte growth factor (HGF) and necroptosis on the proliferation and differentiation of endogenous c-kit+ CSCs in the heart after MI in aged rats. HGF/p-Met expression levels and c-kit+ CSC abundance gradually decreased with age. Adenovirus carrying the HGF gene (Ad-HGF) promoted the differentiation of c-kit+ CSCs into precursors of cardiomyocyte, endothelial, and smooth muscle cell lineages and enhanced cardiomyocyte proliferation and angiogenesis in aged rats. These effects were reversed by inhibiting necroptosis. Ad-HGF administration induced necroptosis by increasing the expression of receptor interacting protein kinase (RIP) 1 and receptor interacting protein kinase (RIP) 3 proteins in infarcted hearts. Furthermore, Ad-HGF-induced necroptosis increased high mobility group box 1 (HMGB1) levels and increased the abundance of c-kit+ cells in the bone marrow, which may partly explain the beneficial effects of necroptosis on c-kit+ CSCs. These findings may help develop new approaches to treat ischemic heart disease in the elderly.
HMGB1 is a DNA-binding protein that is secreted by inflammatory and necrotic cells to the extracellular space and functions as a cytokine. It has been reported that exogenous HMGB1 treatment can induce myocardial regeneration after infarction by enhancing the proliferation and differentiation of cardiac c-kit+ cells. Here, the researchers evaluated the level of HMGB1 protein after Ad-HGF treatment. Compared with the Ad-null treatment group, the expression of HMGB1 in the Ad-HGF treatment group was significantly increased, and Nec-1 effectively inhibited this increase (Figure 1A, B). The serum HMGB1 levels before surgery were similar in the two groups, but the serum HMGB1 levels in the Ad-HGF treatment group were significantly increased, and this change could be effectively reversed by inhibiting necroptosis (Figure 1C). Immunofluorescence staining of bone marrow smears showed that inhibition of necroptosis significantly reduced the number of c-kit+ cells in this tissue induced by Ad-HGF treatment (Figure 1D).
Figure 1. Necroptosis induced by Ad-HGF increased the HMGB1 levels and enhanced the c-kit+ cell number in the bone marrow. (Liu J, et al., 2016)
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The HGF adenoviral particles showed strong expression and bioactivity in my wound healing assays. The viral prep was clean, and the results were highly reproducible. Great product!
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