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Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption.

Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption. Research Abstract Details 

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  • Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption. Abstract Text:

    t kurohaT Kuroha,s takahashiS Takahashi,t komenoT Komeno,k itohK Itoh,t nagasawaT Nagasawa,m yamamotoM Yamamoto,

    Maf recognition elements (MAREs or NF-E2 binding sites) have been shown to be vital for erythroid- and megakaryocyte-specific gene expression. Transcription factor NF-E2 is composed of p45, a large subunit belonging to the CNC family proteins, and a small Maf subunit, and is thought to activate transcription through its binding to MAREs in both the erythroid and megakaryocytic cell lineages. While p45 gene knockout mice exhibit thrombocytopenia due to abnormal terminal differentiation of megakaryocytes, and the mutant mice die of massive bleeding within a week after birth, anemia is not apparent in these animals. Disruption of the nrf2 gene, encoding another CNC family protein, results in no hematological abnormalities. We have therefore tested the hypothesis that Nrf2 might compensate for the p45 deficiency in erythroid lineage cells of p45-knockout mice, thereby masking the anticipated anemia. However, we failed to detect any greater failure in either erythroid or megakaryocytic cell development in Nrf2 plus p45 compound mutant mice as compared to with either individual homozygous mutation. These data suggest that p45 and Nrf2 may both be dispensable for hematopoietic cell development, and that other factors regulate erythroid- and megakaryocyte-specific gene expression through their required MAREs.

    Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption. Publishing Authors By Initials

    t kurohaT Kuroha,s takahashiS Takahashi,t komenoT Komeno,k itohK Itoh,t nagasawaT Nagasawa,m yamamotoM Yamamoto,

    For similar proteins: transcription factors research abstracts see: proteins: transcription factors research

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    Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of biochemistry

    VOLUME: 123

    Page Numbers: 376-9

    Journal Abbreviation: J. Biochem.

    ISSN: 0021-924X

    DAY: 19

    MONTH: Mar

    YEAR: 1998

    Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 376600

    Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption. Keywords Mesh Terms:

    KEYWORDS: Transcription Factors

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption. Information

    Substance Name: Globins

    Registry Number: 9004-22-2

    Grant and Affiliation Information for Ablation of Nrf2 function does not increase the erythroid or megakaryocytic cell lineage dysfunction caused by p45 NF-E2 gene disruption.

    AFFILIATION: Institute of Basic Medical Sciences and Center for TARA, Institute of Clinical Medicine, University of Tsukuba, Tsukuba 305, Japan.

    Country: JAPAN

    JAPAN Research PublicationJAPAN Research Publication

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    MEDLINETA: J Biochem

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