Disease relevance of E2f4

• E2f4-/- mice died of an increased susceptibility to opportunistic infections that appeared to result from craniofacial defects [1].
• We have previously shown that E2f4(-/-) mice display a marked macrocytic anemia implicating E2f4 in the regulation of erythropoiesis [2].

High impact information on E2f4

• We conclude that the macrocytic anemia of E2f4(-/-) mice results primarily from impaired cellular proliferation and that the major role of E2f4 in fetal erythropoiesis is to promote cell cycle progression and cellular proliferation [2].
• E2f4 regulates fetal erythropoiesis through the promotion of cellular proliferation [2].
• We show that loss of E2f4 results in an impaired expansion of the fetal erythroid compartment in vivo that is associated with impaired cell cycle progression and decreased erythroid proliferation [2].

Biological context of E2f4

• In particular, E2f4 has been proposed to be the principal family member responsible for the regulation of cell cycle exit chiefly through its transcriptional repressive properties [2].

Analytical, diagnostic and therapeutic context of E2f4

• Consistent with these observations, cDNA microarray analysis reveals cell cycle control genes as one of the major class of genes down-regulated in E2f4(-/-) FLs, and we provide evidence that E2f4 may directly regulate the transcriptional expression of a number of these genes [2].

References