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Publication : RIG-I plays a critical role in negatively regulating granulocytic proliferation.

First Author  Zhang NN Year  2008
Journal  Proc Natl Acad Sci U S A Volume  105
Issue  30 Pages  10553-8
PubMed ID  18650396 Mgi Jnum  J:139016
Mgi Id  MGI:3807111 Doi  10.1073/pnas.0804895105
Citation  Zhang NN, et al. (2008) RIG-I plays a critical role in negatively regulating granulocytic proliferation. Proc Natl Acad Sci U S A 105(30):10553-8
abstractText  RIG-I has been implicated in innate immunity by sensing intracellular viral RNAs and inducing type I IFN production. However, we have found a significant RIG-I induction in a biological setting without active viral infection-namely, during RA-induced terminal granulocytic differentiation of acute myeloid leukemias. Here, we present evidence that a significant Rig-I induction also occurs during normal myelopoiesis and that the disruption of the Rig-I gene in mice leads to the development of a progressive myeloproliferative disorder. The initiation of progressive myeloproliferative disorder is mainly due to an intrinsic defect of Rig-I(-/-) myeloid cells, which are characterized by a reduced expression of IFN consensus sequence binding protein, a major regulator of myeloid differentiation. Thus, our study reveals a critical regulatory role of Rig-I in modulating the generation and differentiation of granulocytes.
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