PUBLICATION
Sel1l knockdown negatively influences zebrafish embryos endothelium
- Authors
- Barbieri, A., Carra, S., De Blasio, P., Cotelli, F., Biunno, I.
- ID
- ZDB-PUB-171208-7
- Date
- 2017
- Source
- Journal of Cellular Physiology 233(7): 5396-5404 (Journal)
- Registered Authors
- Cotelli, Franco
- Keywords
- Endothelium, Knockdown, Sel1l, Zebrafish
- MeSH Terms
-
- Animals
- Blood Vessels/growth & development
- Blood Vessels/metabolism
- Embryonic Development/genetics*
- Endoplasmic Reticulum/genetics*
- Endoplasmic Reticulum/metabolism
- Endoplasmic Reticulum-Associated Degradation/genetics*
- Endothelium/cytology
- Gene Expression Regulation, Developmental/genetics
- Ubiquitin-Protein Ligases/genetics*
- Zebrafish/genetics
- Zebrafish/growth & development
- Zebrafish Proteins/genetics
- PubMed
- 29215726 Full text @ J. Cell. Physiol.
Citation
Barbieri, A., Carra, S., De Blasio, P., Cotelli, F., Biunno, I. (2017) Sel1l knockdown negatively influences zebrafish embryos endothelium. Journal of Cellular Physiology. 233(7):5396-5404.
Abstract
SEL1L (Suppressor/Enhancer of Lin-12-like) is a highly conserved gene associated with the Endoplasmic Reticulum-Associated Degradation (ERAD) pathway and involved in mediating the balance between stem cells self-renewal and differentiation of neural progenitors. It has been recently shown that SEL1L KO mice are embryonic lethal and display altered organogenesis. To better characterize the function of SEL1L in the early stages of embryonic development, we turned to the zebrafish model (D. rerio). After exploring sel1l expression by RT-PCR and in situ hybridization, we employed a morpholino-mediated down-regulation approach. Results showed extensive impairments in the vasculature, which supports the mice knock-out findings. This article is protected by copyright. All rights reserved.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping