Product Details
Purity |
99%+ |
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2mg 5mg 10mg 15mg 20mg 30me etc. |
Actual peptide content |
Exceed the standard |
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Cleanliness |
Sterile |
Transportation time |
7-15days |
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COA HPLC Third party testing |
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Can provide |
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Resend policy |
According to different countries |
.Aging and many diseases are largely caused by the accumulation of damaged cells that no longer divide. Scientists have found that inhibitors of FOXO4 protein activity can eliminate senescent cells in mice. If a cell is severely damaged, it may enter a self-clearance process called apoptosis or a self-disabling process called senescence. Because senescent cells can survive for a long time, they accumulate in aging and damaged organs. A series of evidence shows that eliminating senescent cells can extend the healthy lifespan of mice and reduce the severity of aging-related diseases. Baar et al.'s paper published in Cell deepens our understanding of this phenomenon. They pointed out that the survival of senescent cells depends on the transcription factor FOXO4. At the same time, mouse models show that tissue dysfunction and age-related diseases caused by chemotherapy can be reversed by pharmacological interference with the function of FOXO4. Senescent cells inhibit their own proliferation ability when reprogrammed, while secreting signaling molecules-a phenomenon called senescence-associated secretory phenotype (SASP). Scientists believe that the normal function of the SASP is to restore tissue function in two ways: first, by stimulating neighboring cells with less damage to participate in tissue repair; second, by attracting inflammatory cells to eliminate senescent cells and shut down SASP-mediated signals. However, this repair process may fail when the extent, duration or frequency of damage exceeds the repair capacity, or when the SASP can no longer stimulate repair and attract inflammatory cells. The end result is an abnormal accumulation of senescent cells and aggravated tissue dysfunction. In the past two years, several studies have shown that because senescent cells have obvious molecular vulnerabilities, they can be targeted for treatment by compounds-these drugs preferentially kill senescent cells. Senescent cells express high levels of pro-apoptotic and anti-apoptotic factors and are therefore always on the verge of cell death. This is the theoretical basis for the preparation of typical anti-aging drugs. These drugs can inhibit the action of the BCL-2 protein family (a class of proteins that promote cell survival) and guide cells into the process of apoptosis. Scientists have also proposed an anti-aging formula based on a combination of two drugs, but the specific molecular basis remains to be elucidated. Gene expression data showed that the transcription factor FOXO4 is upregulated in senescent cells compared with normal cells. Baar further pointed out that downregulation of FOXO4 using inhibitory RNA molecules can trigger apoptosis of senescent cells, but not normal cells, while downregulation of other FOXO family members has no such effect. To some extent, FOXO4 and some of its family members promote cell survival by interacting with multiple protein partners. According to the findings of Baar et al., FOXO4 is an important molecule that promotes the survival of senescent cells. Interestingly, FOXO4 can interact with the protein p53, a known senescence-induced protein. Therefore, the researchers inferred that this FOXO4-p53 interaction may be crucial for the survival of senescent cells, and that disruption of this interaction will promote cell apoptosis (Figure 1). To test this, they synthesized a modified peptide fragment called FOXO4-D reverse transcriptase (FOXO4-DRI). This peptide fragment lacks the normal transcriptional activity of FOXO4, but binds more stably to p53, so it can competitively inhibit the FOXO4-p53 interaction.
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