bp(GO:"erythrocyte differentiation")
These results also indicated that, in spite of enforced extramedullary and medullary erythropoiesis in Ko + Pb mice, erythroid cells did not robustly survive and differentiate under Pb exposure as shown in Table 1, analogous to the observations in cadmium-treated mice.22 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 results also indicated that, in spite of enforced extramedullary and medullary erythropoiesis in Ko + Pb mice, erythroid cells did not robustly survive and differentiate under Pb exposure as shown in Table 1, analogous to the observations in cadmium-treated mice.22 PubMed:25411909
In other words, Hri is necessary for erythroid differentiation and survival under oxidative stress. 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
In other words, Hri is necessary for erythroid differentiation and survival under oxidative stress. PubMed:25411909
These results also indicated that, in spite of enforced extramedullary and medullary erythropoiesis in Ko + Pb mice, erythroid cells did not robustly survive and differentiate under Pb exposure as shown in Table 1, analogous to the observations in cadmium-treated mice.22 PubMed:25411909
These results also indicated that, in spite of enforced extramedullary and medullary erythropoiesis in Ko + Pb mice, erythroid cells did not robustly survive and differentiate under Pb exposure as shown in Table 1, analogous to the observations in cadmium-treated mice.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
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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.