| First Author | Coppin E | Year | 2016 |
| Journal | J Immunol | Volume | 196 |
| Issue | 10 | Pages | 4110-21 |
| PubMed ID | 27183638 | Mgi Jnum | J:319622 |
| Mgi Id | MGI:6859497 | Doi | 10.4049/jimmunol.1501037 |
| Citation | Coppin E, et al. (2016) Dok1 and Dok2 Proteins Regulate Cell Cycle in Hematopoietic Stem and Progenitor Cells. J Immunol 196(10):4110-21 |
| abstractText | Dok1 and Dok2 proteins play a crucial role in myeloid cell proliferation as demonstrated by Dok1 and Dok2 gene inactivation, which induces a myeloproliferative disease in aging mice. In this study, we show that Dok1/Dok2 deficiency affects myeloproliferation even at a young age. An increase in the cellularity of multipotent progenitors is observed in young Dok1/Dok2-deficient mice. This is associated with an increase in the cells undergoing cell cycle, which is restricted to myeloid committed progenitors. Furthermore, cellular stress triggered by 5-fluorouracil (5-FU) treatment potentiates the effects of the loss of Dok proteins on multipotent progenitor cell cycle. In addition, Dok1/Dok2 deficiency induces resistance to 5-FU-induced hematopoietic stem cell exhaustion. Taken together, these results demonstrate that Dok1 and Dok2 proteins are involved in the control of hematopoietic stem cell cycle regulation. |
