TP53Haploinsufficiency Rescues Emergency Granulopoiesis inFANCC−/−Mice
نویسندگان
چکیده
منابع مشابه
Transcriptional Regulation of Emergency Granulopoiesis in Leukemia
Neutropenic conditions are prevalent in leukemia patients and are often associated with increased susceptibility to infections. In fact, emergency granulopoiesis (EG), a process regulating neutrophil homeostasis in inflammatory conditions and infections, may occur improperly in leukemic conditions, leading to reduced neutrophil counts. Unfortunately, the mechanisms central to dysfunctional EG r...
متن کاملIncreased Fanconi C expression contributes to the emergency granulopoiesis response.
Emergency granulopoiesis is a component of the innate immune response that is induced in response to infectious or inflammatory challenge. It is characterized by the rapid expansion and differentiation of granulocyte/monocyte progenitor (GMP) populations, which is due in part to a shortened S-phase of the cell cycle. We found that IRF8 (also known as ICSBP), an interferon regulatory transcripti...
متن کاملHoxA10 Terminates Emergency Granulopoiesis by Increasing Expression of Triad1.
Expression of the E3 ubiquitin ligase Triad1 is greater in mature granulocytes than in myeloid progenitor cells. HoxA10 actives transcription of the gene encoding Triad1 (ARIH2) during myeloid differentiation, but the contribution of increased Triad1 expression to granulocyte production or function is unknown. Mice with bone marrow-specific disruption of the ARIH2 gene exhibit constitutive infl...
متن کاملSTAT3 controls myeloid progenitor growth during emergency granulopoiesis.
Granulocyte colony-stimulating factor (G-CSF) mediates "emergency" granulopoiesis during infection, a process that is mimicked by clinical G-CSF use, yet we understand little about the intracellular signaling cascades that control demand-driven neutrophil production. Using a murine model with conditional deletion of signal transducer and activator of transcription 3 (STAT3) in bone marrow, we i...
متن کاملSTAT3 governs distinct pathways in emergency granulopoiesis and mature neutrophils.
Granulocyte colony-stimulating factor (G-CSF) is essential for the host response to bacterial infection by controlling neutrophil production in the bone marrow. The G-CSF receptor (G-CSFR) activates the Jak/STAT pathway, although little is understood about how these signals regulate basal and stress-induced granulopoiesis. We examined STAT3 function in granulocytes using a bone marrow condition...
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ژورنال
عنوان ژورنال: The Journal of Immunology
سال: 2018
ISSN: 0022-1767,1550-6606
DOI: 10.4049/jimmunol.1700931