| First Author | Martin F | Year | 1998 |
| Journal | Blood | Volume | 91 |
| Issue | 9 | Pages | 3459-66 |
| PubMed ID | 9558405 | Mgi Jnum | J:47440 |
| Mgi Id | MGI:1203443 | Doi | 10.1182/blood.v91.9.3459.3459_3459_3466 |
| Citation | Martin F, et al. (1998) Erythroid maturation and globin gene expression in mice with combined deficiency of NF-E2 and nrf-2. Blood 91(9):3459-66 |
| abstractText | NF-E2 binding sites, located in distant regulatory sequences, may be important for high level alpha- and beta-globin gene expression. Surprisingly, targeted disruption of each subunit of NF-E2 has either little or no effect on erythroid maturation in mice. For p18 NF-E2, this lack of effect is due, at least in part, to the presence of redundant proteins. For p45 NF-E2, one possibility is that NF-E2- related factors, Nrf-1 or Nrf-2, activate globin gene expression in the absence of NF-E2. To test this hypothesis for Nrf-2, we disrupted the Nrf-2 gene by homologous recombination. Nrf-2-deficient mice had no detectable hematopoietic defect. In addition, no evidence was found for reciprocal upregulation of NF-E2 or Nrf-2 protein in fetal liver cells deficient for either factor. Fetal liver cells deficient for both NF-E2 and Nrf-2 expressed normal levels of alpha- and beta-globin. Mature mice with combined deficiency of NF-E2 and Nrf-2 did not exhibit a defect in erythroid maturation beyond that seen with loss of NF-E2 alone. Thus, the presence of a mild erythroid defect in NF-E2-deficient mice is not the result of compensation by Nrf-2. |
