■细胞生长涉及细胞分裂。这在达到一定限制后停止。一些细胞变得无活性并且不能经历凋亡(程序性细胞死亡)。这些细胞积聚在组织损伤或疾病的部位,从而加速衰老。它们被称为衰老细胞。已经开发了可以消除衰老细胞(senolyics)或抑制其有害作用(senomorphics)的治疗性干预措施。衰老(老化)是由叉头(FHD)和反式激活(TAD)域之间的分子间和分子内相互作用引起的,以及C末端区域3(CR3)和DNA结合(DBD)。另一方面,抗衰老/衰老(抗衰老)活性是通过破坏这些与CR3-和叉头框蛋白O4(FOXO4)为基础的肽的相互作用来实现的,例如ES2和DRI,分别。在这项研究中,我们使用基于数字信号处理的计算机化程序来系统分析senoletics及其靶标之间的分子间相互作用。
■采用信息频谱法(ISM)。
■我们从CR3和FOXO4的相互作用蛋白中获得了肽的序列,并评估了它们破坏FOXO4和DRI以及CR3和BDB之间分子间相互作用的能力,负责衰老(衰老)。我们的结果表明,这些肽具有不同程度的衰老(抗衰老)活性,取决于它们对CR3和BDB的亲和力,或者FOXO4和DRI.我们发现增强衰老2(ES2)对CR3和BDB的亲和力高于FOXO4和DRI,CR3和BDB之间的相互作用对衰老至关重要。因此,ES2和其他基于CR3的肽比基于FOXO4的肽更有效。我们的发现与以前的研究一致,并揭示了衰老和衰老机制的新见解。ES2被认为是最好的抗衰老候选物,因为它比DRI有效3-7倍。我们验证了ES2与FOXO4的相互作用比CR3弱。然而,DRI的性能取决于其分子内相互作用和稳定性。因此,使用基于数字信号处理的技术进行分子内分析已变得非常重要,并且将随之而来。
■基于CR3的肽是用于抗衰老疗法的有希望的候选物。senoletics是氨基酸的线性链,可以靶向和消除衰老细胞,这些细胞已经停止分裂并导致衰老和与年龄有关的疾病。通过使用这个建议,基于数字信号处理的新型计算机技术,senolyics可以很容易地分析和优化其有效性和安全性。通过提供可以延缓或逆转衰老的干预措施以及可以推进老年学领域的见解,这为提高我们的寿命和福祉提供了更合理的方法。这个过程也将补充其他方法,如分子刺激,等。
UNASSIGNED: Cell growth involves cell division. This stops after reaching a certain limit. Some cells become inactive and unable to undergo apoptosis (programmed cell death). These cells accumulate at sites of tissue damage or disease, thus accelerating aging. They are called senescent cells. Therapeutic interventions that can either eliminate senescent cells (senolytics) or suppress their harmful effects (
senomorphics) have been developed. Senescence (aging) is caused by the inter- and intramolecular interactions between the domains of forkhead (FHD) and transactivation (TAD), as well as C-terminal region 3 (CR3) and DNA binding (DBD). On the other hand, anti-senescent/senolytic (anti-aging) activities are achieved by disrupting these interactions with CR3- and forkhead box protein O4 (FOXO4)-based peptides, such as ES2 and DRI, respectively. In this study, we use a computerized procedure based on digital signal processing to systematically analyze the inter-molecular interactions between senolytics and their targets.
UNASSIGNED: Informational spectrum method (ISM) is engaged.
UNASSIGNED: We obtained the sequences of the peptides from the interacting proteins of CR3 and FOXO4 and evaluated their ability to disrupt the inter-molecular interactions between FOXO4 and DRI and CR3 and BDB, which are responsible for senescence (aging). Our results show that the peptides have different degrees of senolytic (anti-aging) activity, depending on their affinity for CR3 and BDB, or FOXO4 and DRI. We found that enhanced senescence 2 (ES2) has a higher affinity for CR3 and BDB than FOXO4 and DRI, and that the interaction between CR3 and BDB is crucial for aging. Therefore, ES2 and other CR3-based peptides are more potent senolytics than FOXO4-based peptides. Our findings are consistent with previous studies and reveal new insights into the mechanisms of senescence and senolytics. ES2 is considered the best senolytic candidate, as it is 3-7 times more effective than DRI. We verified that ES2 has a weaker interaction with FOXO4 than CR3. However, the performance of DRI has been noted to depend on its intramolecular interactions and stability. Hence, intramolecular analyses using the digital signal processing-based technique has become very vital and will follow.
UNASSIGNED: CR3-based peptides are promising candidates for senolytic therapy. Senolytics are linear chains of amino acids that can target and eliminate senescent cells, which are cells that have stopped dividing and contribute to aging and age-related diseases. By using this proposed, novel computerized technique that is based on digital signal processing, senolytics can be easily analyzed and optimized for their effectiveness and safety. This provides a more rational approach to enhancing our longevity and well-being by offering interventions that can delay or reverse aging and insights that can advance the field of gerontology. This procedure also will compliment other approaches such as molecular stimulation, etc.