Transient arrest in a quiescent state allows ovarian cancer cells to survive suboptimal growth conditions and is mediated by both Mirk/dyrk1b and p130/Rb2

LKB1 and AMP-activated protein kinase control of mTOR signalling and growth

(2009) R. J. Shaw   Acta Physiologica

Mirk/Dyrk1B Maintains the Viability of Quiescent Pancreatic Cancer Cells by Reducing Levels of Reactive Oxygen Species

(2009) X. Deng et al.   CANCER RESEARCH

Cancer Stem Cells and Aneuploid Populations within Developing Tumors Are the Major Determinants of Tumor Dormancy

(2009) A. P. Kusumbe et al.   CANCER RESEARCH

Computational Identification of a p38SAPK-Regulated Transcription Factor Network Required for Tumor Cell Quiescence

(2009) A. P. Adam et al.   CANCER RESEARCH

Mirk Regulates the Exit of Colon Cancer Cells from Quiescence

(2009) Kideok Jin et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Hijacking HES1: how tumors co-opt the anti-differentiation strategies of quiescent cells

(2009) Liyun Sang et al.   TRENDS IN MOLECULAR MEDICINE

G0Function of BCL2 and BCL-xLRequires BAX, BAK, and p27 Phosphorylation by Mirk, Revealing a Novel Role of BAX and BAK in Quiescence Regulation

(2008) Yelena Janumyan et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

TSC–mTOR maintains quiescence and function of hematopoietic stem cells by repressing mitochondrial biogenesis and reactive oxygen species

(2008) Chong Chen et al.   JOURNAL OF EXPERIMENTAL MEDICINE

Control of the Reversibility of Cellular Quiescence by the Transcriptional Repressor HES1

(2008) L. Sang et al.   SCIENCE