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Literature summary for 1.13.11.31 extracted from

  • Weisinger, G.; Grafi-Cohen, M.; Hirsh, M.; Knoll, E.; Sharon, O.; Many, A.; Limor, R.; Stern, N.
    12S-Lipoxygenase is necessary for human vascular smooth muscle cell survival (2013), Exp. Cell Res., 319, 1586-1593 .
    View publication on PubMed
Search for more literature for 1.13.11.31

Inhibitors

Inhibitors Comment Organism Structure
baicalein the 12LO inhibitor induces a 2-2.5fold increase in cell death, which appears to result from apoptosis, as indicated by DNA fragmentation, activation of procaspase 3 to caspase 3 and cytochrome c release from the mitochondria to the cytosol. This apoptosis can be prevented by treatment with the 12LO product, 12 hydroxyeicosatetraenoic acid (12HETE) Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
arachidonate + O2 Homo sapiens
-
 (5Z,8Z,10E,14Z)-(12S)-12-hydroperoxyicosa-5,8,10,14-tetraenoate
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens P18054
-
-

Source Tissue

Source Tissue Comment Organism Textmining
blood platelet
-
 Homo sapiens
-
vascular smooth muscle cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
arachidonate + O2
-
 Homo sapiens (5Z,8Z,10E,14Z)-(12S)-12-hydroperoxyicosa-5,8,10,14-tetraenoate
-
 ?

Synonyms

Synonyms Comment Organism
12LO
-
 Homo sapiens
12S-lipoxygenase
-
 Homo sapiens
2-lipoxygenase
-
 Homo sapiens
ALOX12
-
 Homo sapiens
platelet-type 12LO
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction the 12LO inhibitor induces a 2-2.5fold increase in cell death, which appears to result from apoptosis, as indicated by DNA fragmentation, activation of procaspase 3 to caspase 3 and cytochrome c release from the mitochondria to the cytosol. Human platelet-type 12LO-antisense knockdown, by either plasmid transfection or adeno-associated virus (AAV) infection also induces substantial VSMC death over controls, which can also be prevented by treatment with 12HETE, but not 5HETE. Hence, biochemical 12LO inhibition or 12LO-antisense knockdown in VSMC can induce programmed cell death Homo sapiens
physiological function 12-lipoxygenase (12LO) is a dioxygenase enzyme that incorporates molecular oxygen into unsaturated fatty acids such as arachidonic acid at carbon position 12. Arachidonate LOs and their products play an important role in mediating growth factor induced tumor cell proliferation and appear to enhance the growth and migration of vascular smooth muscle cells, VSMC. VSMC proliferation is essential in vascular wall function as well as plaque formation and the inhibition of the renin angiotensin system can induce VSMC apoptosis Homo sapiens