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Central point: c-Myc controls the self-renewal, stillness, and survival of HSC by adjusting the expressions of Nr4a1, Nr4a2, and Jmjd3.
Apc haploxic dose deficiency is lost by increasing the secretion of IL6 in c-Myc-mediated bone marrow endothelial cells to prevent red line differentiation.
: A new study published recently in the journal Blood reports on the dose effects of c-Myc on hematopoietic effects and its unique role in the hematopoietic stem cell (HSC) and bone marrow niche cell brokering Wnt/b-catenin path.
researchers found that inadequate doses of c-Myc monolithics can lead to ineffective hemaging by inhibiting HSC self-renewal and rest and promoting apoptosis, and also found three genes, Nr4a1, Nr4a2 and Jmjd3, which are c-Myc's downstream targets in HSC that are critical to maintaining HSC function.
c-Myc is directly integrated with the initiation subregions of Nr4a1, Nr4a2, and Jmjd3 to regulate its expression.
all three genes are involved in the maintenance function of c-Myc for HSC survival, and Nr4a1 and Nr4a2 also mediat c-Myc's regulation of HSC stationary function.
the tumor suppressor Apc is a negative regulatory factor in the Wnt/b-catenin path path.
first time, researchers have found that insufficient doses of Apc monohyma can induce red line differentiation block by promoting bone marrow endothort cell expression and secretion of IL-6.
and insufficient dose of c-Myc monolithic can not restore the functional defects of Apc-defective HSC in the body, but can effectively prevent the development of severe anemia in mice with Apc hybrid type, significantly prolonging the survival of such mice.
in addition, the researchers demonstrated that c-Myc-mediated endoblast cellSap is induced by IL-6 secretion, and that insufficient dose of c-Myc monolithic can reverse the negative effect of Apc defective endoskin cells on erythre cell differentiation.
, the study shows that c-Myc has an up-and-down effect in mediating Apc's function in hemaging.
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