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Title: Functional characterization of a mammalian transcription factor, Elongin A

Abstract

Elongin A is the transcriptionally active subunit of the Elongin complex that strongly stimulates the rate of elongation by RNA polymerase II (pol II) by suppressing the transient pausing of the polymerase at many sites along the DNA template. We have recently shown that Elongin A-deficient mice are embryonic lethal, and mouse embryonic fibroblasts (MEFs) derived from Elongin A{sup -/-} embryos display not only increased apoptosis but also senescence-like phenotypes accompanied by the activation of p53. To further understand the function of Elongin A in vivo, we have carried out the structure-function analysis of Elongin A and identified sequences critical to its nuclear localization and direct interaction with pol II. Moreover, we have analyzed the replication fork movement in wild-type and Elongin A{sup -/-} MEFs, and shown the possibility that the genomic instability observed in Elongin A{sup -/-} MEFs might be caused by the replication fork collapse due to Elongin A deficiency.

Authors:
 [1];  [2];  [3];  [4];  [3];  [2];  [5]
  1. Department of Functional Genomics, Kochi Medical School, Kohasu, Oko-cho, Nankoku, Kochi 783-8505 (Japan)
  2. Laboratory of Molecular and Cellular Biology, Faculty of Bioresources, Mie University, 1515 Kamihama, Tsu, Mie 514-8507 (Japan)
  3. Department of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo 113-8510 (Japan)
  4. Microbial Chemistry Research Foundation, Kamiosaki, Shinagawa-ku, Tokyo 141-0021 (Japan)
  5. Department of Functional Genomics, Kochi Medical School, Kohasu, Oko-cho, Nankoku, Kochi 783-8505 (Japan). E-mail: asot@med.kochi-u.ac.jp
Publication Date:
OSTI Identifier:
20857950
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 352; Journal Issue: 1; Other Information: DOI: 10.1016/j.bbrc.2006.11.012; PII: S0006-291X(06)02466-1; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; DNA; ELONGATION; EMBRYOS; FIBROBLASTS; IN VIVO; INSTABILITY; INTERACTIONS; MICE; PHENOTYPE; RNA; STRUCTURE FUNCTIONS; TRANSCRIPTION; TRANSCRIPTION FACTORS

Citation Formats

Yasukawa, Takashi, Sugimura, Kazuto, Fukuda, Mizue, Yamazaki, Katsuhisa, Kitajima, Shigetaka, Okumura, Katsuzumi, and Aso, Teijiro. Functional characterization of a mammalian transcription factor, Elongin A. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2006.11.012.
Yasukawa, Takashi, Sugimura, Kazuto, Fukuda, Mizue, Yamazaki, Katsuhisa, Kitajima, Shigetaka, Okumura, Katsuzumi, & Aso, Teijiro. Functional characterization of a mammalian transcription factor, Elongin A. United States. doi:10.1016/j.bbrc.2006.11.012.
Yasukawa, Takashi, Sugimura, Kazuto, Fukuda, Mizue, Yamazaki, Katsuhisa, Kitajima, Shigetaka, Okumura, Katsuzumi, and Aso, Teijiro. Fri . "Functional characterization of a mammalian transcription factor, Elongin A". United States. doi:10.1016/j.bbrc.2006.11.012.
@article{osti_20857950,
title = {Functional characterization of a mammalian transcription factor, Elongin A},
author = {Yasukawa, Takashi and Sugimura, Kazuto and Fukuda, Mizue and Yamazaki, Katsuhisa and Kitajima, Shigetaka and Okumura, Katsuzumi and Aso, Teijiro},
abstractNote = {Elongin A is the transcriptionally active subunit of the Elongin complex that strongly stimulates the rate of elongation by RNA polymerase II (pol II) by suppressing the transient pausing of the polymerase at many sites along the DNA template. We have recently shown that Elongin A-deficient mice are embryonic lethal, and mouse embryonic fibroblasts (MEFs) derived from Elongin A{sup -/-} embryos display not only increased apoptosis but also senescence-like phenotypes accompanied by the activation of p53. To further understand the function of Elongin A in vivo, we have carried out the structure-function analysis of Elongin A and identified sequences critical to its nuclear localization and direct interaction with pol II. Moreover, we have analyzed the replication fork movement in wild-type and Elongin A{sup -/-} MEFs, and shown the possibility that the genomic instability observed in Elongin A{sup -/-} MEFs might be caused by the replication fork collapse due to Elongin A deficiency.},
doi = {10.1016/j.bbrc.2006.11.012},
journal = {Biochemical and Biophysical Research Communications},
number = 1,
volume = 352,
place = {United States},
year = {Fri Jan 05 00:00:00 EST 2007},
month = {Fri Jan 05 00:00:00 EST 2007}
}