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Literature summary for 1.13.11.33 extracted from

  • Suzuki, H.; Kayama, Y.; Sakamoto, M.; Iuchi, H.; Shimizu, I.; Yoshino, T.; Katoh, D.; Nagoshi, T.; Tojo, K.; Minamino, T.; Yoshimura, M.; Utsunomiya, K.
    Arachidonate 12/15-lipoxygenase-induced inflammation and oxidative stress are involved in the development of diabetic cardiomyopathy (2015), Diabetes, 64, 618-630.
    View publication on PubMed
Search for more literature for 1.13.11.33

Application

Application Comment Organism
medicine the enzyme is a target in treatment of cardiomyopathy Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information generation of Alox15-deficient (12/15-LOX KO) mice Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
cinnamyl-3,4-dihydroxy-cyanocinnamate
-
 Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
arachidonate + O2 Mus musculus
-
 (5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate
-
 ?
arachidonate + O2 Mus musculus C57BL/6
-
 (5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate
-
 ?

Organism

Organism UniProt Comment Textmining
Mus musculus P39654
-
-
Mus musculus C57BL/6 P39654
-
-

Source Tissue

Source Tissue Comment Organism Textmining
cardiomyocyte
-
 Mus musculus
-
heart expression of 12/15-LOX pathway is upregulated in the diabetic heart Mus musculus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
arachidonate + O2
-
 Mus musculus (5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate
-
 ?
arachidonate + O2
-
 Mus musculus C57BL/6 (5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate
-
 ?

Synonyms

Synonyms Comment Organism
12/15-LOX
-
 Mus musculus
Alox15
-
 Mus musculus
arachidonate 12/15-lipoxygenase
-
 Mus musculus
cardiac 12/15-LOX
-
 Mus musculus

Expression

Organism Comment Expression
Mus musculus expression of 12/15-LOX pathway is upregulated in the diabetic heart up

General Information

General Information Comment Organism
malfunction streptozotocin (STZ)-induced diabetic mice show upregulated expression of 12/15-LOX and inflammatory cytokines such as tumor necrosis factor (TNF)-alpha and nuclear factor (NF)-kappaB in diabetic hearts. Disruption of 12/15-LOX significantly improves STZ-induced cardiac dysfunction and fibrosis. Deletion of 12/15-LOX inhibits the increases of TNF-alpha and NF-kappaB as well as the production of STZ-induced reactive oxygen species in the heart. Administration of N-acetylcysteine in diabetic mice prevents STZ-induced cardiac fibrosis. Neonatal cultured cardiomyocytes exposed to high glucose conditions induce the expression of 12/15-LOX as well as TNF-alpha, NF-kappaB, and collagen markers. These increases are inhibited by treatment of the 12/15-LOX inhibitor. Disruption of 12/15-LOX reduces inflammation, oxidative stress, and fibrosis in the diabetic heart, thereby improving systolic dysfunction. Disruption of 12/15-LOX decreases cardiac inflammation induced by hyperglycemia Mus musculus
metabolism cardiac 12/15-LOX pathway induced by high glucose condition increases the expression of cardiac inflammation in vitro Mus musculus
physiological function cardiac 12/15-LOX-induced inflammation and oxidative stress are involved in the development of diabetic cardiomyopathy. 12/15-LOX induces cardiac oxidative stress in the diabetic heart Mus musculus