PUBLICATION
Traffic jams in fish bones: ER-to-Golgi protein transport during zebrafish development
- Authors
- Melville, D.B., and Knapik, E.W.
- ID
- ZDB-PUB-110103-7
- Date
- 2011
- Source
- Cell adhesion & migration 5(2): 114-118 (Review)
- Registered Authors
- Knapik, Ela W., Melville, David
- Keywords
- none
- MeSH Terms
-
- Animals
- COP-Coated Vesicles/genetics
- COP-Coated Vesicles/metabolism*
- Carrier Proteins/metabolism
- Embryo, Nonmammalian
- Endoplasmic Reticulum/metabolism*
- Gene Expression Regulation, Developmental
- Golgi Apparatus/metabolism*
- Humans
- Protein Transport
- Saccharomyces cerevisiae Proteins/metabolism
- Vesicular Transport Proteins/genetics
- Vesicular Transport Proteins/metabolism*
- Zebrafish/embryology
- Zebrafish/metabolism
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 21178403 Full text @ Cell Adh. Migr.
Citation
Melville, D.B., and Knapik, E.W. (2011) Traffic jams in fish bones: ER-to-Golgi protein transport during zebrafish development. Cell adhesion & migration. 5(2):114-118.
Abstract
Extracellular matrix (ECM) proteins, cell adhesion molecules, cytokines, morphogens and membrane receptors are synthesized in the ER and transported through the Golgi complex to the cell surface and the extracellular space. The first leg in this journey from the ER to Golgi is facilitated by the Coat Protein II (COPII) vesicular carriers. Genetic defects in genes encoding various COPII components cause a broad spectrum of human diseases, from anemia to skeletal deformities. Here, we summarize our findings in zebrafish and discuss how mutations in COPII elements may cause specific cellular and developmental defects.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping