1
This element was shown to enhance ABO promoter activity in an erythroid cell-specific manner.
2
Recent studies suggest that decreased erythroid cell differentiation and survival also contribute to IE, aggravating the anemia in BT.
3
These findings indicate that the suppression of miRNA-451a or miRNA-486-5p might be associated with the benzene-induced perturbation of erythroid cell differentiation.
4
However, information about the catabolism of heme in erythroid cells is limited.
5
We conclude that normal Ikaros function increases normal apoptosis in erythroid cells.
6
Erythroid cells undergo enucleation and the removal of organelles during terminal differentiation.
7
Bone marrow is generally considered the main source of erythroid cells.
8
This receptor is expressed by subsets of endothelial, as well as erythroid cells.
9
Finally, sustained expression of alternative FPN1 transcripts is apparently observed only in erythroid cells.
10
This phenotype clearly differs from that induced by tyrosine kinase oncogenes in erythroid cells.
11
Expression of globin genes in developing erythroid cells is controlled by upstream locus control regions.
12
FOG-1 suppressed the proliferation of primitive and definitive erythroid cells in all stages of differentiation.
13
We have previously shown that DMT1 deficiency impairs erythroid differentiation and induces apoptosis of erythroid cells.
14
The aim of this study was to investigate whether erythroid cells possess specific mechanisms for iron export.
15
In 16 younger adults and children, erythroid cells and platelets were predominantly derived from normal stem cells.
16
Nucleated erythroid cells had high expression of ACKR1, which facilitated their direct contact with hematopoietic stem cells.