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Modification of kidney barrier function by the urokinase receptor

signalling in podocytes causes foot process effacement and urinary protein loss. The mechanism responsible includes the lipid-dependent activation of , as scientists from the Harvard Medical School in Boston (USA) showed.

Podocyte dysfunction, characterised by the symptoms caused by signalling, is often preceding progressive kidney disease.

The research team observed, that mice lacking intact (-/-) did not develop -mediated proteinuria in the first place but the disease appeared after expression of a constitutively active .
are required in podocytes for cell motility and activation of the small GTPases and via activation of . If is blocked in vitro, podocyte motility decreases, but the blockage lowers proteinuria in mice.
The seems to fulfil a physiological role in the regulation of kidney permeability. Nonetheless, therapies attacking at the cellular level of the disease are currently not available.

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