Part:BBa_K5063000
Ginsentide TP1 coding sequence
Ginseng is a medicinal plant that has been used for centuries in traditional medicine systems, particularly in Asia. It is available in different species, with Asian ginseng (Panax ginseng) and American ginseng (Panax quinquefolius) being the most commonly used. Ginseng is known for its adaptogenic properties, believed to help the body cope with stress and promote overall well-being. Ginsentides are different from ginsenosides, they share similarity in certain bioactive functions but differ in magnitude. Ginsentides are disulphide-rich, cell-penetrating and proteolytic-stable microproteins. It reduces phenylephrine-induced vasoconstriction.Ginsentides, similar to other cysteine-rich peptides, including roseltides, bleogens, chenotides, and avenatides, are structurally constrained by multiple disulfides to render them resistant to proteolytic degradation, making them potentially orally active. The cell-penetrating superdisulfide peptides or microproteins such as ginsentides would have advantages over unconstrained peptides. Ginsentide and ginsentide-like peptides would also have an advantage over small-molecule metabolites whose footprints are too small to inhibit intracellular protein interactions.
Ginsentide TP1 Enhancing Production of Nitric Oxide TP1 enhances the production of endothelial nitric oxide (NO) via the PI3K/Akt/eNOS pathway, which contributes to their cardiovascular advantages. Several studies have highlighted the vasodilatory and blood pressure-lowering effects of ginseng extracts, mainly through the elevation of NO levels. NO is essential for dilating blood vessels and ensuring proper vascular tone.
NO diffuses into surrounding smooth muscle cells, significantly influencing vascular function. Once inside these cells, NO activates guanylate cyclase, which catalyses the conversion of guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP). This second messenger is vital for various cellular processes, including the dephosphorylation of myosin light chains, which regulates muscle contraction.
Dephosphorylation leads to the dissociation of myosin from actin filaments, resulting in the relaxation of smooth muscle cells. This relaxation causes blood vessels to dilate, effectively lowering blood pressure and mitigating hypertension. By reducing hypertension, Ginsentide TP1 offers protective effects against endothelial damage, thereby lowering the overall risk of atherosclerosis. This mechanism highlights the importance of NO in maintaining vascular health and underscores the cardiovascular benefits associated with ginsentides.
Ginsentide TP1 Inhibiting P2Y12 Receptor Ginsentide TP1 inhibits the P2Y12 receptor (P2Y12r) on platelets, which is a G protein-coupled receptor that plays a crucial role in platelet activation and aggregation. It is activated by adenosine diphosphate (ADP), which is released from activated platelets and other cells. When ADP binds to the P2Y12 receptor, it triggers a signalling cascade that leads to platelet activation, enhancing their ability to aggregate and form clots. Ginsentide prevents ADP from binding to these receptors. This inhibition effectively blocks platelet activation and aggregation. As a result, the rate of platelet aggregation is significantly lowered, which can reduce thrombus formation.
We have found that only targeting atherosclerosis and thrombosis is not enough, we decided to tackle the problem from another perspective, which is targeting the plasma LDL level.
Effect of TP1 on Low-density Lipoprotein Low-density lipoprotein (LDL) plays a critical role in atherosclerosis and thrombosis through various mechanisms. Elevated LDL levels in the bloodstream can accumulate in arterial walls, particularly in areas with compromised endothelial linings, marking the onset of atherosclerosis. LDL undergoes oxidation to form oxidised LDL (oxLDL), which triggers inflammatory responses and attracts immune cells like macrophages. These cells engulf oxLDL, transforming into foam cells that create fatty streaks, developing into larger plaques that narrow arteries and restrict blood flow.
Furthermore, oxLDL activates platelets through interactions with two key receptors: cluster of differentiation 36 (CD36) and lectin-like oxidised low-density lipoprotein receptor-1 (LOX1). These interactions enhance platelet activation and aggregation, contributing to thrombus formation and the inflammatory processes associated with atherosclerosis. Thus, effective management strategies for LDL are essential in preventing cardiovascular disease.
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21COMPATIBLE WITH RFC[21]
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000COMPATIBLE WITH RFC[1000]
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