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Literature summary for 3.3.2.10 extracted from

  • Luo, P.; Chang, H.H.; Zhou, Y.; Zhang, S.; Hwang, S.H.; Morisseau, C.; Wang, C.Y.; Inscho, E.W.; Hammock, B.D.; Wang, M.H.
    Inhibition or deletion of soluble epoxide hydrolase prevents hyperglycemia, promotes insulin secretion, and reduces islet apoptosis (2010), J. Pharmacol. Exp. Ther., 334, 430-438.
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
gGenotyping for Ephx2-/-, Ephx2+/-, and Ephx2+/+ mice, overview Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information Ephx2-/- mice, sEH knockout and its inhibition prevent hyperglycemia in diabetes, but also that sEH knockout enhances islet GSIS through the amplifying pathway and decreases islet cell apoptosis in diabetes. sEH knockout increases Ca2+ response to high glucose and KCl plus diazoxide, and it reduces islet cell apoptosis in streptozotocin-treated mice Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
trans-4-[4-(3-adamantan-1-ylureido)-cyclohexyloxy]-benzoic acid i.e. t-AUCB Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
soluble
-
Mus musculus
-
-

Organism

Organism UniProt Comment Textmining
Mus musculus P34914 C57BL/6J mice
-
Mus musculus C57/BL6J P34914 C57BL/6J mice
-

Source Tissue

Source Tissue Comment Organism Textmining
heart
-
Mus musculus
-
kidney
-
Mus musculus
-
liver
-
Mus musculus
-
additional information sEH tissue distribution, no activity in lung, overview Mus musculus
-
pancreatic islet
-
Mus musculus
-
spleen
-
Mus musculus
-

General Information

General Information Comment Organism
malfunction sEH knockout and its inhibition prevent hyperglycemia in diabetes, and sEH knockoit also enhances islet GSIS through the amplifying pathway and decreases islet cell apoptosis in diabetes, overview Mus musculus
physiological function sEH is an enzyme involved in the metabolism of endogenous inflammatory and antiapoptotic mediators Mus musculus