MIDA1, a Protein Associated with Id, Regulates Cell Growth (*)

  1. Wataru Shoji,
  2. Toshiaki Inoue,
  3. Tohru Yamamoto(§) and
  4. Masuo Obinata(¶)
  1. From the Department of Cell Biology, Institute of Development, Aging, and Cancer, Tohoku University, 4-1 Seiryomachi Aoba-ku, Sendai 980-77, Japan
  1. To whom correspondence should be addressed. Tel.: 81-22-274-1111 (ext. 3461); Fax: 81-22-272-5081.
  • § Present address: Inst. of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 102, Japan.

Abstract

We have isolated cDNA clone encoding a protein that can associate with Id, a helix-loop-helix (HLH) protein. This protein is named MIDA1 (mouse Id associate 1), and its predicted amino acid sequence consists of Zuotin (a putative Z-DNA binding protein in yeast) homology region and tryptophan-mediated repeats similar to c-Myb oncoprotein. MIDA1 associates with the HLH region of Id with the conserved region adjacent to eukaryotic DnaJ conserved motif within the Zuotin homology region, although it does not have any canonical HLH motif. The addition of antisense oligonucleotide of MIDA1 inhibited growth of murine erythroleukemia cells without interfering with erythroid differentiation, indicating that it regulates cell growth.

Footnotes

  • * The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore by hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    The nucleotide sequence(s) reported in this paper has been submitted to the GenBank™/EMBL Data Bank with accession number(s) D63784[GenBank].

  • 1 The abbreviations used are:

    HLH

    helix-loop-helix

    bHLH

    basic HLH

    MEL

    murine erythroleukemia

    GST

    glutathione S-transferase

    PAGE

    polyacrylamide gel electrophoresis

    PBS

    phosphate-buffered saline

    BrdU

    5-bromo-2′-deoxyuridine.

  • 2W. Shoji and M. Obinata, unpublished data.

  • 3S. Ishii, personal communication.

    • Received June 14, 1995.
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