Journal
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
Volume 16, Issue 12, Pages 3543-3552Publisher
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2005030240
Keywords
-
Categories
Funding
- NCI NIH HHS [R24CA095823] Funding Source: Medline
- NIDDK NIH HHS [P01 DK62345, F32DK10130] Funding Source: Medline
Ask authors/readers for more resources
The human protein kinase X (PRKX) gene was identified previously as a cAMP-dependent serine/threonine kinase that is aberrantly expressed in autosomal dominant polycystic disease kidneys and normally expressed in fetal kidneys. The PRKX kinase belongs to a serine/threonine kinase family that is phylogenetically and functionally distinct from classical protein kinase A kinases. Expression of PRKX activates cAMP-dependent renal epithelial cell migration and tubular morphogenesis in cell culture, suggesting that it might regulate branching growth of the collecting duct system in the fetal kidney. With the use of a mouse embryonic kidney organ culture system that recapitulates early kidney development in vitro, it is demonstrated that lentiviral vector-driven expression of a constitutively active, cAMP-independent PRKX in the ureteric bud epithelium stimulates branching morphogenesis and results in a 2.5-fold increase in glomerular number. These results is suggest that PRKX stimulates epithelial branching morphogenesis by activating cell migration and support a role for this kinase in the regulation of nephrogenesis and of collecting system development in the fetal kidney.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available