PUBLICATION
Dishevelled2 is a stable protein during early zebrafish development
- Authors
- Lum, W.M., Robertson, J.K., and Van Raay, T.J.
- ID
- ZDB-PUB-110628-1
- Date
- 2011
- Source
- Zebrafish 8(2): 65-71 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Adaptor Proteins, Signal Transducing/chemistry
- Adaptor Proteins, Signal Transducing/genetics
- Adaptor Proteins, Signal Transducing/metabolism*
- Amino Acid Sequence
- Animals
- Carrier Proteins/genetics
- Carrier Proteins/metabolism
- Gene Expression Regulation, Developmental
- Humans
- Molecular Sequence Data
- Phosphoproteins/chemistry
- Phosphoproteins/genetics
- Phosphoproteins/metabolism*
- Proteasome Endopeptidase Complex/metabolism
- Sequence Alignment
- Signal Transduction
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 21663448 Full text @ Zebrafish
Citation
Lum, W.M., Robertson, J.K., and Van Raay, T.J. (2011) Dishevelled2 is a stable protein during early zebrafish development. Zebrafish. 8(2):65-71.
Abstract
Wnt signaling is a major player during development and its misregulation often leads to disease, especially cancer. The negative feedback Wnt regulator homologs, Nkd1 and Nkd2, have been shown to inhibit Wnt signaling during development, and current evidence suggests that Nkds degrade Dvl proteins to antagonize Wnt signaling. Here, we demonstrate that during early zebrafish development Nkd1 does not alter either endogenous or exogenous levels of Dvl2. Furthermore, Dvl2 does not affect the levels of Nkd1. Cumulatively, these results demonstrate that Dvl2 is a ubiquitous and stable protein and that Nkds may not always function to degrade Dvl proteins as a method of inhibiting Wnt signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping