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CAT# | Product Name | M.W | Molecular Formula | Inquiry |
---|---|---|---|---|
U03001 | (Pyr-110)-Prepro-Urotensin II (110-123) (rat) | 1663.90 | C77H102N18O20S2 | Inquiry |
U03002 | Urotensin II-Related Peptide (human, mouse, rat) | C49H64N10O10S2 | Inquiry | |
U03003 | Urotensin II, human | 1390.6 | Inquiry | |
U03004 | Urotensin II, rat, [pGlu110] - Prepro - Urotensin II (110 - 123), rat | 1663.9 | Inquiry | |
U03007 | Urotensin II (Frog) | 1517.76 | C69H96N16O19S2, | Inquiry |
U03009 | (Pyr1)-Urotensin II (rat) | 1663.90 | C₇₇H₁₀₂N₁₈O₂₀S₂ | Inquiry |
U03010 | Orn8, Urotensin II, human | 1374.6 | C63H83N13O18S2 | Inquiry |
U03012 | Urotensin II , goby | 1361.57 | C₆₂H₈₄N₁₄O₁₇S₂ | Inquiry |
U03014 | Urotensin II-Related Peptide (human, mouse, rat) trifluoroacetate salt | 1017.24 | C₄₉H₆₄N₁₀O₁₀S₂ | Inquiry |
Urotensin-II (U-II) is the strongest vasopressin ligand known. Because the U-II system is involved in many biological systems, such as the cardiovascular system, nervous system, endocrine system, and kidney system, it is a promising target for the development of new drugs. Human Urotensin Ⅱ (hU-Ⅱ) is a polypeptide composed of 11 amino acids. The primary structure of Glu-Thr-Pro-Asp-cyclo [Cys-Phe-Trp-Lys-Tyr-Cys]-Val, is the strongest vasoconstrictor peptide known so far. Its C-terminal highly conserved hexapeptide structure Cys-Phe-Trp-Lys-Tyr-Cys is very similar to SST and OCT. U-II plays a vasoactive role by binding to its specific receptor GPR14. It has been found that SST and OCT can also compete to bind to the GPR14 receptor at high concentration and inhibit the vasoconstrictive activity of U-II.
U-II plays a vasoactive role by binding to its specific orphan G-protein coupling receptor GPR-14. The vasoactive effect of U-II is race-specific and disease-specific. With the further study of U-II, it is found that U-II not only has vascular activity but also has the effect of promoting mitosis and fibrosis. It has been found that the expression of U-II is increased in plasma of patients with liver cirrhosis, but its role in the occurrence and development of chronic liver disease and portal hypertension. The mechanism is not yet clear.
U-II has different effects on different tissues. It can cause a contraction in blood vessels. In rat pancreas, U-II inhibits insulin secretion. It also affects the kidneys, including sodium transport, lipid, and glucose metabolism, and natriuretic action. It is associated with cardiac fibrosis and hypertrophy, heart failure, renal insufficiency, and diabetes. The increased expression of U-II and its receptor UT in the cirrhotic portal vein is closely related to the severity of the disease and complications such as ascetic fluid. However, the specific mechanism of U-II/UT system in the occurrence and development of cirrhotic portal vein disease is not clear. The application of U-II receptor antagonist can improve the hemodynamic disorder of portal hypertension and prevent hepatic fibrosis, suggesting that U-II receptor antagonist may be an important tool for the prevention and treatment of cirrhotic portal hypertension. The role in cirrhotic portal hypertension can provide a new idea for the treatment of cirrhotic portal hypertension.
References
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