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Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression.

Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression. Research Abstract Details 

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  • Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression. Abstract Text:

    Multifunctional transcription factor TFII-I has two spliced isoforms (Delta and beta) in murine fibroblasts. Here we show that these isoforms have distinct subcellular localization and mutually exclusive transcription functions in the context of growth factor signaling. In the absence of signaling, TFII-Ibeta is nuclear and recruited to the c-fos promoter in vivo. But upon growth factor stimulation, the promoter recruitment is abolished and it is exported out of the nucleus. Moreover, isoform-specific silencing of TFII-Ibeta results in transcriptional activation of the c-fos gene. In contrast, TFII-IDelta is largely cytoplasmic in the resting state but translocates to the nucleus upon growth factor signaling, undergoes signal-induced recruitment to the same site on the c-fos promoter, and activates the gene. Importantly, activated TFII-IDelta interacts with Erk1/2 (MAPK) kinase in the cell cytoplasm and imports the Erk1/2 to the nucleus, thereby transducing growth factor signaling. Our results identify a unique growth factor signaling pathway controlled by opposing activities of two TFII-I spliced isoforms.

    Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression. Publishing Authors By Initials

    For similar proteins: dna-binding proteins: transcription factors, general: transcription factors, tfii research abstracts see: proteins: dna-binding proteins: transcription factors, general: transcription factors, tfii research

    PUBMED ID PMID:

    MEDLINE DATE:

    Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression. Journal Published:

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

    Journal: Molecular cell

    VOLUME: 24

    Page Numbers: 301-8

    Journal Abbreviation: Mol. Cell

    ISSN: 1097-2765

    DAY: 20

    MONTH: Oct

    YEAR: 2006

    Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9802571

    Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression. Keywords Mesh Terms:

    KEYWORDS: Transcription Factors, TFII

    MESH TERMS: chemistry

    Chemical & Substance for Abstract: Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression. Information

    Substance Name: Transcription Factors, TFII

    Registry Number: 0

    Grant and Affiliation Information for Opposing functions of TFII-I spliced isoforms in growth factor-induced gene expression.

    AFFILIATION: Program in Immunology, Tufts University School of Medicine, 150 Harrison Avenue, Boston, Massachusetts 02111, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIGMS

    GRANT: R37-GM34277

    ACRONYM: GM

    MEDLINETA: Mol Cell

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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