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

BRENDA support

Literature summary for 3.2.1.166 extracted from

  • Masola, V.; Zaza, G.; Secchi, M.F.; Gambaro, G.; Lupo, A.; Onisto, M.
    Heparanase is a key player in renal fibrosis by regulating TGF-beta expression and activity (2014), Biochim. Biophys. Acta, 1843, 2122-2128.
    View publication on PubMed

Protein Variants

Protein Variants Comment Organism
additional information reduced enzyme expression in enzyme-silenced cells Homo sapiens

Inhibitors

Inhibitors Comment Organism Structure
low molecular weight heparin
-
Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
epithelium
-
Homo sapiens
-
HK-2 cell
-
Homo sapiens
-
kidney
-
Homo sapiens
-
mesenchyme
-
Homo sapiens
-
renal tubule
-
Homo sapiens
-

Synonyms

Synonyms Comment Organism
HPSE
-
Homo sapiens

Temperature Optimum [°C]

Temperature Optimum [°C] Temperature Optimum Maximum [°C] Comment Organism
37
-
assay at Homo sapiens

pH Optimum

pH Optimum Minimum pH Optimum Maximum Comment Organism
7.4
-
assay at Homo sapiens

Expression

Organism Comment Expression
Homo sapiens no effect by TGF-beta on the enzyme expression in enzyme-silenced cells additional information

General Information

General Information Comment Organism
malfunction the lack of heparanase or its inhibition prevents the increased synthesis of TGF-beta by tubular cells in response to pro-fibrotic stimuli such as FGF-2, advanced glycosylation end products and albumin overload. TGF-beta induces an autocrine loop to sustain its signal, whereas the lack of the enzyme partially interferes with this autocrine loop Homo sapiens
physiological function heparanase is a key player in renal fibrosis by regulating TGF-beta expression and activity, overview. Heparanase is an endo-beta-D-glucuronidase that cleaves heparan-sulfate thus regulating the bioavailability of growth factors (FGF-2, TGF-beta). The enzyme controls FGF-2-induced epithelial-mesenchymal transition in tubular cells and is necessary for the development of diabetic nephropathy in mice. Homo sapiens