Journal of the American Society of Nephrology
2007 JASN IMPACT FACTOR 7.111 HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP 
    advanced
CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION


Published ahead of print on October 19, 2005
J Am Soc Nephrol 16: 3543-3552, 2005
© 2005 American Society of Nephrology
doi: 10.1681/ASN.2005030240

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
ASN.2005030240v1
16/12/3543    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Li, X.
Right arrow Articles by Burrow, C. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Li, X.
Right arrow Articles by Burrow, C. R.
Related Collections
Right arrowRelated Article

Genetics and Development

Protein Kinase X Activates Ureteric Bud Branching Morphogenesis in Developing Mouse Metanephric Kidney

Xiaohong Li, Deborah P. Hyink, Katalin Polgar, G. Luca Gusella, Patricia D. Wilson and Christopher R. Burrow

Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, New York, New York

Address correspondence to: Dr. Patricia D. Wilson, Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029. Phone: 212-659-9376; Fax: 212-849-2434; pat.wilson{at}mssm.edu

Received for publication March 2, 2005. Accepted for publication September 4, 2005.

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 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.


Related Article

This Month’s Highlights
J. Am. Soc. Nephrol. 2005 16: 3447-3448. [Full Text] [PDF]






HOME CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP