Synergistic cooperation of Sall4 and Cyclin D1 in transcriptional repression

Johann Böhm, Frank J. Kaiser, Wiktor Borozdin, Reinhard Depping, Jürgen Kohlhase

21 Citations (Scopus)


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 G1 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.

Original languageEnglish
JournalBiochemical and Biophysical Research Communications
Issue number3
Pages (from-to)773-779
Number of pages7
Publication statusPublished - 11.05.2007

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)


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