PUBLICATION

Snrk-1 is involved in multiple steps of angioblast development and acts via notch signaling pathway in artery-vein specification in vertebrates

Authors
Chun, C.Z., Kaur, S., Samant, G.V., Wang, L., Pramanik, K., Garnaas, M.K., Li, K., Field, L., Mukhopadhyay, D., and Ramchandran, R.
ID
ZDB-PUB-080902-5
Date
2009
Source
Blood   113(5): 1192-1199 (Journal)
Registered Authors
Field, Lyndsay, Garnaas, Maija, Ramchandran, Ramani
Keywords
none
Datasets
GEO:GSE12516
MeSH Terms
  • Animals
  • Arteries/embryology*
  • Basic Helix-Loop-Helix Transcription Factors/genetics
  • Basic Helix-Loop-Helix Transcription Factors/metabolism
  • Cell Movement/physiology
  • Endothelial Cells/enzymology
  • Gene Expression Regulation, Developmental/physiology*
  • Gene Expression Regulation, Enzymologic/physiology*
  • Gene Knockdown Techniques
  • Humans
  • Oligonucleotide Array Sequence Analysis
  • Protein Serine-Threonine Kinases/biosynthesis*
  • Protein Serine-Threonine Kinases/genetics
  • Receptors, Notch/genetics
  • Receptors, Notch/metabolism
  • Veins/embryology*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
18723694 Full text @ Blood
Abstract
In vertebrates, molecular mechanisms dictate angioblasts' migration and subsequent differentiation into arteries and veins. In this study, we used a microarray screen to identify a novel member of the sucrose non-fermenting related kinase (snrk-1) family of serine/threonine kinases expressed specifically in the embryonic zebrafish vasculature and investigated its function in vivo. Using gain and loss of function studies in vivo, we show that Snrk-1 plays an essential role in the migration, maintenance and differentiation of angioblasts. The kinase function of Snrk-1 is critical for migration and maintenance, but not for the differentiation of angioblasts. In vitro, snrk-1 knockdown endothelial cells show only defects in migration. The snrk-1 gene acts downstream or parallel to notch and upstream of gridlock during artery-vein specification, and the human gene compensates for zebrafish snrk-1 knockdown, suggesting evolutionary conservation of function.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping