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Genetic Structure and Chromosomal Mapping of Myd88

  1. Author:
    Hardiman, G.
    Jenkins, N. A.
    Copeland, N. G.
    Gilbert, D. J.
    Garcia, D. K.
    Naylor, S. L.
    Kastelein, R. A.
    Bazan, J. F.
  2. Author Address

    Bazan JF DNAX RES INST MOL & CELLULAR BIOL INC DEPT MOL BIOL PALO ALTO, CA 94304 USA DNAX RES INST MOL & CELLULAR BIOL INC DEPT MOL BIOL PALO ALTO, CA 94304 USA NCI FREDERICK CANC RES & DEV CTR ABL BASIC RES PROGRAM MAMMALIAN GENET LAB FREDERICK, MD 21702 USA UNIV TEXAS HLTH SCI CTR DEPT CELLULAR & STRUCT BIOL SAN ANTONIO, TX 78284 USA
    1. Year: 1997
  1. Journal: Genomics
    1. 45
    2. 2
    3. Pages: 332-339
  2. Type of Article: Article
  1. Abstract:

    The myeloid differentiation (MyD) marker MyD88 was initially characterized as a primary response gene, upregulated in mouse M1 myeloleukemic cells in response to differentiation induced by interleukin-6. Subsequent analysis revealed that MyD88 possesses a unique modular structure, which consists of an N-terminal ''death domain,'' similar to the intracellular segments of TNF receptor 1 and Fas, and a C-terminal region related to the cytoplasmic domains of the Drosophila morphogen Toll and vertebrate interleukin-l receptors. In this report we describe the cloning and gene structure of mouse MyD88. The complete coding sequence of mouse MyD88 spans five exons, with the first exon encoding the complete death domain. Zoo-blot analysis revealed that MyD88 is an evolutionarily conserved gene. MyD88 was localized to the distal region of mouse chromosome 9 by interspecific backcross mapping. The human homolog (hMyD88) was mapped to chromosome 3p22-p21.3 by PCR analysis of a human chromosome 3 somatic cell hybrid mapping panel. Northern blot analysis revealed widespread expression of MyD88 in many adult mouse tissues, and RT-PCR studies detected MyD88 mRNA in T and B cell lines and differentiating embryonic stem cells. The broad expression pattern demonstrates that mouse MyD88 expression is not restricted to cells of myeloid lineage as was originally believed. (C) 1997 Academic Press. [References: 43]

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