Synergistic cooperation of Sall4 and Cyclin D1 in transcriptional repression
- Institut fuer Humangenetik und Anthropologie, Universitaet Freiburg, Freiburg (Germany)
- Institut fuer Humangenetik, Universitaetsklinikum Schleswig-Holstein, Campus Luebeck (Germany)
- Institut fuer Physiologie, Universitaet zu Luebeck, Luebeck (Germany)
- Institut fuer Humangenetik und Anthropologie, Universitaet Freiburg, Freiburg (Germany) and Praxis fuer Humangenetik, Heinrich-von-Stephan-Str. 5, 79100 Freiburg (Germany)
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{sub 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.
- OSTI ID:
- 20991337
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 356, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2007.03.050; PII: S0006-291X(07)00522-0; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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