p(MGI:Eif2ak1)
Moreover, in the current study, we identified a crucial role of Hri in protecting erythroid precursors during differentiation by promoting terminal maturation including enucleation, preventing cell death, and increasing iron availability for erythropoiesis. PubMed:25411909
These data suggested that Pb-induced anemia should be ascribed to (at least partially) Pbinduced death of erythrocytes, and also stressed the critical role of Hri in assuring the survival of BM and spleen erythroid cells under Pb exposure. PubMed:25411909
Hri is activated to protect cells from oxidative stress-provoked apoptosis upon arsenic, cadmium, and iron deficiency.18,19,22 PubMed:25411909
These findings together led us to postulate that there could be disordered differentiation and survival for Hri-deficient erythroid cells upon Pb exposure. PubMed:25411909
These results are similar to our findings in an earlier study where Hri deficiency resulted in the blockade of erythroid differentiation of FL cells from early and late basophilic erythroblasts into chromatophilic and orthochromatophilic erythroblasts.19 PubMed:25411909
These results suggest that Pb elicits direct inhibition of erythroid cell differentiation and that more importantly Hri takes a crucial role in promoting erythroid differentiation in response to Pb-induced toxicity. PubMed:25411909
These data together demonstrated that Pb caused the inhibition of erythroid enucleation and that Hri seemingly surveilled the terminal differentiation of erythroblasts for appropriate hemoglobin production and final maturation before enucleation. PubMed:25411909
Our combined results revealed that Hri functions to protect erythroid cells from Pb-induced toxicity through enhancing erythroid differentiation, enforcing cell survival, and orchestrating iron homeostasis. PubMed:25411909
Moreover, in the current study, we identified a crucial role of Hri in protecting erythroid precursors during differentiation by promoting terminal maturation including enucleation, preventing cell death, and increasing iron availability for erythropoiesis. PubMed:25411909
Moreover, loss of Hri gave rise to hepatic hepcidin induction, associated with iron retention in spleens. PubMed:25411909
Under Pb administration, Wt mice did not develop phenotypes of anemia; however, Hri-deficient mice developed severe anemia. PubMed:25411909
These findings together led us to postulate that there could be disordered differentiation and survival for Hri-deficient erythroid cells upon Pb exposure. PubMed:25411909
These results are similar to our findings in an earlier study where Hri deficiency resulted in the blockade of erythroid differentiation of FL cells from early and late basophilic erythroblasts into chromatophilic and orthochromatophilic erythroblasts.19 PubMed:25411909
These results suggest that Pb elicits direct inhibition of erythroid cell differentiation and that more importantly Hri takes a crucial role in promoting erythroid differentiation in response to Pb-induced toxicity. PubMed:25411909
These data together demonstrated that Pb caused the inhibition of erythroid enucleation and that Hri seemingly surveilled the terminal differentiation of erythroblasts for appropriate hemoglobin production and final maturation before enucleation. PubMed:25411909
Our combined results revealed that Hri functions to protect erythroid cells from Pb-induced toxicity through enhancing erythroid differentiation, enforcing cell survival, and orchestrating iron homeostasis. PubMed:25411909
These data suggested that Pb-induced anemia should be ascribed to (at least partially) Pbinduced death of erythrocytes, and also stressed the critical role of Hri in assuring the survival of BM and spleen erythroid cells under Pb exposure. PubMed:25411909
Hri is activated to protect cells from oxidative stress-provoked apoptosis upon arsenic, cadmium, and iron deficiency.18,19,22 PubMed:25411909
Under Pb administration, Wt mice did not develop phenotypes of anemia; however, Hri-deficient mice developed severe anemia. PubMed:25411909
Moreover, in the current study, we identified a crucial role of Hri in protecting erythroid precursors during differentiation by promoting terminal maturation including enucleation, preventing cell death, and increasing iron availability for erythropoiesis. PubMed:25411909
Moreover, in the current study, we identified a crucial role of Hri in protecting erythroid precursors during differentiation by promoting terminal maturation including enucleation, preventing cell death, and increasing iron availability for erythropoiesis. PubMed:25411909
Moreover, loss of Hri gave rise to hepatic hepcidin induction, associated with iron retention in spleens. PubMed:25411909
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.