Deficiency of the zinc finger protein ZPR1 causes defects in transcription and cell cycle progression
Authors
Gangwani, LaxmanUMass Chan Affiliations
Program in Molecular MedicineDocument Type
Journal ArticlePublication Date
2006-10-28Keywords
Carrier ProteinsCell Cycle
Cell Cycle Proteins
Cell Line
Cell Survival
DNA Replication
G1 Phase
G2 Phase
Hela Cells
Histones
Humans
Intranuclear Space
Motor Neurons
Nuclear Proteins
Organelles
S Phase
*Transcription, Genetic
Zinc Fingers
Life Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
The zinc finger protein ZPR1 is present in both the cytoplasm and nucleoplasm. Cell cycle analysis demonstrates that ZPR1 undergoes major changes in subcellular distribution during proliferation. ZPR1 is diffusely localized throughout the cell during the G(1) and G(2)/M phases of the cell cycle. In contrast, ZPR1 redistributes to the nucleus during S phase and ZPR1 exhibits prominent co-localization with the survival motor neurons protein and the histone gene-specific transcription factor NPAT in subnuclear foci, including Cajal bodies that associate with histone gene clusters. ZPR1 deficiency causes disruption of survival motor neurons and NPAT localization within the nucleus, blocks S phase progression, and arrests cells in both the G(1) and G(2) phases of the cell cycle. These changes in subnuclear architecture and cell cycle progression may be caused by transcriptional defects in ZPR1-deficient cells, including decreased histone gene expression.Source
J Biol Chem. 2006 Dec 29;281(52):40330-40. Epub 2006 Oct 26. Link to article on publisher's siteDOI
10.1074/jbc.M608165200Permanent Link to this Item
http://hdl.handle.net/20.500.14038/42312PubMed ID
17068332Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1074/jbc.M608165200