Synergistic Cooperation of Sall4 and Cyclin D1 in Transcriptional Repression.
From: Institut für Humangenetik und Anthropologie, Universität Freiburg, Freiburg, Germany.
Biochemical and biophysical research communications
- Publish Date: May 2007
- ISSN: 0006-291X
- Volume: 356
- Issue: 3
- Pages: 773-9
- Medium: Print
- Language: English
- Citation (JAMA): Böhm Johann, Kaiser Frank J, Borozdin Wiktor, et al. Synergistic Cooperation of Sall4 and Cyclin D1 in Transcriptional Repression.. Biochem. Biophys. Res. Commun. May 2007;356:773-9
Abstract
Loss of function mutations in SALL4 cause Okihiro syndrome, an autosomal dominant disorder characterised by radial ray malformations associated with Duane anomaly. In zebrafish and mouse Sall4 interacts with TBX5 during limb and heart development and plays a crucial role for embryonic stem (ES) cell pluripotency. Here we report the nuclear interaction of murine Sall4 with Cyclin D1, one of the main regulators of G(1) to S phase transition in cell cycle, verified by yeast two-hybrid assay, co-immunoprecipitation and intracellular co-localisation. Furthermore, using luciferase reporter gene assays we demonstrate that Sall4 operates as a transcriptional repressor located to heterochromatin and that this activity is modulated by Cyclin D1.
Mesh Headings (Keywords): Animals, COS Cells, Cell Nucleus, Cercopithecus aethiops, Cyclins, DNA-Binding Proteins, Mice, Repressor Proteins, Transcription Factors, Transcription, Genetic
Check for Full Text / PubMed Unique Identifier (PMID): 17383611
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