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Exchange of N-CoR corepressor and Tip60 coactivator complexes links gene expression by NF-kappaB and beta-amyloid precursor protein.

Defining the molecular mechanisms that integrate diverse signaling pathways at the level of gene transcription remains a central issue in biology. Here, we demonstrate that interleukin-1beta (IL-1beta) causes nuclear export of a specific N-CoR corepressor complex, resulting in derepression of a specific subset of NF-kappaB-regulated genes, exemplified by the tetraspanin KAI1 that regulates membrane receptor function. Nuclear export of the N-CoR/TAB2/HDAC3 complex by IL-1beta is temporally linked to selective recruitment of a Tip60 coactivator complex. Surprisingly, KAI1 is also directly activated by a ternary complex, dependent on the acetyltransferase activity of Tip60, consisting of the presenilin-dependent C-terminal cleavage product of the amyloid beta precursor protein (APP), Fe65, and Tip60, identifying a specific in vivo gene target of an APP-dependent transcription complex in the brain.

Pubmed ID: 12150997


  • Baek SH
  • Ohgi KA
  • Rose DW
  • Koo EH
  • Glass CK
  • Rosenfeld MG



Publication Data

July 12, 2002

Associated Grants


Mesh Terms

  • Acetyltransferases
  • Active Transport, Cell Nucleus
  • Adaptor Proteins, Signal Transducing
  • Amino Acid Sequence
  • Amyloid beta-Protein Precursor
  • Animals
  • Antigens, CD
  • Antigens, CD82
  • Carrier Proteins
  • Cells, Cultured
  • Cercopithecus aethiops
  • Histone Acetyltransferases
  • Humans
  • Interleukin-1
  • MAP Kinase Kinase Kinase 1
  • Membrane Glycoproteins
  • Molecular Sequence Data
  • NF-kappa B
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Nuclear Receptor Co-Repressor 1
  • Promoter Regions, Genetic
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins
  • RNA, Messenger
  • Repressor Proteins
  • Signal Transduction
  • Up-Regulation