PUBLICATION
Znf45l affects primitive hematopoiesis by regulating transforming growth factor-beta signaling
- Authors
- Chen, H., Sun, H., Tao, D., Yang, P., Bian, S., Liu, Y., Zhang, S., and Ma, Y.
- ID
- ZDB-PUB-131218-10
- Date
- 2014
- Source
- BMB reports 47(1): 21-6 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Embryo, Nonmammalian/metabolism
- Embryonic Development
- Morpholines/metabolism
- Phosphorylation
- Protein Serine-Threonine Kinases/metabolism
- RNA Interference
- RNA, Messenger/metabolism
- Receptors, Transforming Growth Factor beta/metabolism
- Signal Transduction
- Transforming Growth Factor beta/metabolism*
- Zebrafish/growth & development
- Zebrafish Proteins/antagonists & inhibitors
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 24209630 Full text @ BMB Rep.
Citation
Chen, H., Sun, H., Tao, D., Yang, P., Bian, S., Liu, Y., Zhang, S., and Ma, Y. (2014) Znf45l affects primitive hematopoiesis by regulating transforming growth factor-beta signaling. BMB reports. 47(1):21-6.
Abstract
Znf45l, containing classical C2H2 domains, is a novel member of Zinc finger proteins in zebrafish. In vertebrates, TGF-β signaling plays a critical role in hematopoiesis. Here, we showed that Znf45l is expressed both maternally and zygotically throughout early development. Znf45l-depleted Zebrafish embryos display shorter tails and necrosis with reduced expression of hematopoietic maker genes. Furthermore, we revealed that znf45l locates downstream of TGF-β ligands and maintains normal level of TGF-β receptor typeaphosphorylation. In brief, our results indicate that znf45l affects initial hematopoietic development through regulation of TGF-β signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping