Erythroid-enriched BMP2K kinase, in addition to its predicted function in endocytosis, regulates distribution and abundance of COPII assemblies and autophagic degradation through opposing actions of its two splicing variants.

Erythroid maturation-dependent remodelling of CTLH E3 complex, along with its cognate E2, controls the orderly progression of human erythropoiesis, thus establishing a paradigm for other E2-E3 ubiquitylation modules involved in developmental processes.

Mouse fetal liver macrophages that support erythroid differentiation within erythroblastic islands exhibit a unique and transient expression signature under transcriptional control of EKLF/KLF1.

An RNA-regulatory machine confers expression and function of a receptor tyrosine kinase to dictate a developmental signaling transition.

The heme and HRI-mediated eIF2aP–ATF4 integrated stress response in erythropoiesis has a major global impact, especially under the stress condition of iron deficiency.

Erythropoietin transiently remodels the hematopoietic stem and progenitor cells pool by directly inducing myeloid-erythroid-megakaryocyte-biased multipotent progenitor clones compensated at the population level by induction of myeloid-B-cell-dendritic-cell-biased clones.

Increased extramedullary erythropoiesis in spleen compensates for the elevated turnover of red blood cells in mice lacking CD47, but extramedullary erythropoiesis is suppressed in mice lacking the CD47 ligand thrombospondin-1.

Ras-GAP activity suppresses the hemogenic potential of the embryonic heart.

Genetic complementation approaches in a mouse model of anemia reveals new protein interactions which aid cell survival and promote sensing of environmental cues.

The expansion of our understanding about the regulation of iron metabolism, erythropoiesis, and the crosstalk between them has enabled delineating the pathophysiology of multiple diseases and provided rationale for novel therapeutic interventions.