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A situation may be created which the phenotypes observed in classical Nur77-KO mice can be a much less severe type of the fast-onset AML phenotype observed in Nur77 and NOR-1 double-knockout mice, which Screen splenomegaly, skewing of HSPCs toward myeloid progeny, and critical bone marrow defects inside 21 times (seven).
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Nur77 regulates various elements of hematopoiesis and relevant pathologies, such as monocyte differentiation (6) and AML (seven). Whilst its steps for a transcription variable are founded in these procedures, somewhat tiny BIO77 is known with regards to the job of nongenomic Nur77 action while in the bone marrow.
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These observations lend credence to the idea that the human TR3β transcript variant exists and that it has a Organic purpose unique from that of total-size Nur77. In addition, our analyses recommend a role for TR3β in AML and KRAS signaling (Fig. 5, B