Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary extracted from

  • Vlodavsky, I.; Blich, M.; Li, J.P.; Sanderson, R.D.; Ilan, N.
    Involvement of heparanase in atherosclerosis and other vessel wall pathologies (2013), Matrix Biol., 32, 241-251.
    View publication on PubMedView publication on EuropePMC

Activating Compound

EC Number Activating Compound Comment Organism Structure
3.2.1.166 angiotensin II
-
 Homo sapiens
3.2.1.166 oxidized LDL
-
 Homo sapiens
3.2.1.166 palmitic acid palmitic acid-induced nuclear entry of heparanase facilitates heparan sulfate cleavage Homo sapiens

Inhibitors

EC Number Inhibitors Comment Organism Structure
3.2.1.166 heparin
-
 Homo sapiens
3.2.1.166 M402 a glycol-split heparin compound similar to SST0001 yet smaller in molecular mass Homo sapiens
3.2.1.166 PG545
-
 Homo sapiens
3.2.1.166 PI-88
-
 Homo sapiens
3.2.1.166 SST0001
-
 Homo sapiens

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
3.2.1.166 nucleus palmitic acid triggers lysosome permeabilization, nuclear shuttling of released heparanase by Hsp90 Homo sapiens 5634
-

Organism

EC Number Organism UniProt Comment Textmining
3.2.1.166 Homo sapiens
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
3.2.1.166 blood vessel wall
-
 Homo sapiens
-
3.2.1.166 coronary artery heparanase expression in coronary artery disease Homo sapiens
-
3.2.1.166 macrophage
-
 Homo sapiens
-
3.2.1.166 additional information heparanase is up-regulated in essentially all human tumors examined Homo sapiens
-

Expression

EC Number Organism Comment Expression
3.2.1.166 Homo sapiens heparanase is up-regulated in essentially all human tumors examined. Oxidized lipid- or angiotensin-induced expression of heparanase in macrophages may be a primary mechanism increasing heparanase in atherosclerotic plaques up

General Information

EC Number General Information Comment Organism
3.2.1.166 physiological function heparanase, the sole mammalian endoglycosidase degrading heparan sulfate, is causally involved in cancer metastasis, angiogenesis, inflammation and kidney dysfunction. Involvement of heparanase in atherosclerosis and other vessel wall pathologies, overview. Heparanase promotes thrombosis after vascular injury and contributes to a pro-coagulant state in human carotid atherosclerosis. Heparanase emerges as a regulator of vulnerable lesion development and potential target for therapeutic intervention in atherosclerosis and related vessel wall complications. The enzyme plays a direct role of heparanase in tumor metastasis. heparanase promotes gene expression (i.e., VEGF, tissue factor, HGF, RANKL, TNFalpha) and signaling pathways (i.e., phosphorylation of Akt, Src, Erk, EGF-receptor, insulin receptor) of which some are mediated by its C-terminus domain, devoid of heparanase enzymatic activity. Heparanase activates macrophages via Toll-like receptor similar to the marked increase of TNFalpha and IL-1 following addition of heparanase to monocytes isolated from human peripheral blood. Molecular mechanism underlying cytokine induction by heparanase, overview. Heparanase alters arterial structure and repair following endovascular stenting. The enzyme is a potent regulator of vascular remodeling, both on the level of paracrine regulation of vascular homeostasis and as an effector molecule in vascular response to injury Homo sapiens