These Epor knock-out mice exhibit embryonic lethality with severe anemia. They are suitable for use in applications related to the study of hematopoiesis.
Leonard I. Zon, Children's Hospital
Mice lacking Epor died in utero at embryonic day 11 - 12.5 with severe anemia. Embryonic erythropoiesis was markedly diminished, while fetal liver hematopoiesis was blocked at the proerythroblast stage. Homozygotes are not viable.
|Allele Name||targeted mutation 1, Leonard I Zon|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Epor, erythropoietin receptor|
|Strain of Origin||129S4/SvJae|
|Molecular Note||A genomic fragment containing the splice acceptor site of exon 2 and all of exon 3 was replaced with a neomycin selection cassette. RT-PCR analysis on E12 peripheral blood of homozygous E12 embryos demonstrated that no detectable transcript was produced from this allele.|
|Mutations Made By|| |
Leonard Zon, Children's Hospital
When maintaining a live colony, heterozygous mice may be bred to wildtype siblings. Homozygotes are not viable.
When using the EpoR- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003213 in your Materials and Methods section.