Cat.No. : AD00218Z
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. | AD00218Z |
| Target Gene | NR4A3 |
| Species | Human |
| Product Type | Adenoviral particle |
| Insert | NR4A3 |
| 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 | NR4A3 nuclear receptor subfamily 4, group A, member 3 [ Homo sapiens ] |
| Gene Symbol | NR4A3 |
| Synonyms | CHN; TEC; CSMF; NOR1; MINOR |
| Gene ID | 8013 |
| UniProt ID | Q92570 |
| mRNA Refseq | NM_006981.3 |
| Protein Refseq | NP_008912.2 |
| Chromosome Location | 9q22 |
| Function | DNA binding; RNA polymerase II core promoter proximal region sequence-specific DNA binding transcription factor activity involved in positive regulation of transcription; sequence-specific DNA binding; steroid hormone receptor activity; thyroid hormone receptor activity; zinc ion binding; |
| Pathway | Gene Expression, organism-specific biosystem; Generic Transcription Pathway, organism-specific biosystem; Nuclear Receptor transcription pathway, organism-specific biosystem; Transcriptional misregulation in cancer, organism-specific biosystem; Transcriptional misregulation in cancer, conserved biosystem; |
| MIM | 600542 |
Immediate early gene nuclear receptor subfamily 4, group A, member 3 (Nr4a3) has been implicated in a variety of cellular processes. However, its role and underlying mechanisms in ischemia-reperfusion (IR) remain unknown. Here, researchers show that Nr4a3 expression is upregulated in the heart after IR and that cardiac-specific Nr4a3 deficiency protects against myocardial ischemic injury and improves cardiac function. Overexpression of Nr4a3 in neonatal and adult mouse hearts is sufficient to induce left ventricular dilation and systolic dysfunction without additional ischemic stress. Mechanistically, ischemia or hypoxia triggers Nr4a3 phosphorylation and translocation from the nucleus to the mitochondria, where it interacts with Bnip3 and promotes Bnip3 integration into the mitochondrial membrane. This integration leads to mitochondrial permeability transition pore (mPTP) opening and a reduction in the mitochondrial permeability transition pore (ΔΨm), which results in cardiomyocyte apoptotic and necrotic death.
Experimental evidence suggests that both ischemia- and hypoxia-induced cardiac injury induce cardiomyocyte death through necroptosis and apoptosis, leading to maladaptive remodeling and heart failure. To further investigate the important role of Nr4a3 in hypoxia-induced cell death, researchers performed PI (propidium iodide) and TUNEL staining to detect necrotic and apoptotic cell death in cardiomyocytes in vitro. They found that Nr4a3 knockdown significantly reduced the rates of necrotic and apoptotic cell death after hypoxia-reoxygenation (HR) injury (Figure 1A to D). Knockdown of Nr4a3 by siRNA was accompanied by downregulation of cleaved caspase 3 expression in hypoxic cardiomyocytes (Figure 1E). In contrast, overexpression of Nr4a3 by adenoviral vector (Ad-Nr4a3) in cultured cardiomyocytes resulted in extensive cell necrosis and apoptosis under both normoxic and hypoxic conditions (Figure 1F to I). Therefore, these results suggest that Nr4a3 is required for hypoxia-induced cardiomyocyte death.
Figure 1. Nr4a3 is critically involved in cardiomyocyte necrotic and apoptotic cell death. (Zhang H, et al. 2021)
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