Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Circ Res. 2009 Jun 5;104(11):1260-6. doi: 10.1161/CIRCRESAHA.108.191718. Epub 2009 May 7.

Genetic evidence for a noncanonical function of seryl-tRNA synthetase in vascular development.

Author information

  • 1Department of Biochemistry and Biophysics and the Cardiovascular Research Institute, Programs in Developmental Biology, Genetics, and Human Genetics, University of California, San Francisco, San Francisco, CA 94158, USA.

Erratum in

  • Circ Res. 2009 Oct 23;105(9):e54.

Abstract

In a recent genetic screen, we identified mutations in genes important for vascular development and maintenance in zebrafish (Jin et al. Dev Biol. 2007;307:29-42). Mutations [corrected] at the adrasteia (adr) locus cause a pronounced dilatation of the aortic arch vessels as well as aberrant patterning of the hindbrain capillaries and, to a lesser extent, intersomitic vessels. This dilatation of the aortic arch vessels does not appear to be caused by increased cell proliferation but is dependent on vascular endothelial growth factor (Vegf) signaling. By positional cloning, we isolated seryl-tRNA synthetase (sars) as the gene affected by the adr mutations. Small interfering RNA knockdown experiments in human umbilical vein endothelial cell cultures indicate that SARS also regulates endothelial sprouting. These analyses of zebrafish and human endothelial cells reveal a new noncanonical function of Sars in endothelial development.

PMID:
19423847
[PubMed - indexed for MEDLINE]
PMCID:
PMC2726715
Free PMC Article

Images from this publication.See all images (4)Free text

Figure 1
Figure 2
Figure 3
Figure 4
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk