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The intracellular domain of Notch ligand Delta1 induces cell growth arrest
Author(s) -
Kolev Vihren,
Kacer Doreen,
Trifonova Radiana,
Small Deena,
Duarte Maria,
Soldi Raffaella,
Graziani Irene,
Sideleva Olga,
Larman Barry,
Maciag Thomas,
Prudovsky Igor
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.09.042
Subject(s) - intracellular , notch signaling pathway , microbiology and biotechnology , transmembrane protein , notch 1 , cleavage (geology) , transmembrane domain , notch proteins , chemistry , biology , signal transduction , receptor , biochemistry , paleontology , fracture (geology)
Notch signaling involves proteolytic cleavage of the transmembrane Notch receptor after binding to its transmembrane ligands, Delta or Jagged; and the resultant soluble intracellular domain of Notch stimulates a cascade of transcriptional events. The Delta1 ligand also undergoes proteolytic cleavage upon Notch binding, resulting in the production of a free intracellular domain. We demonstrate that the expression of the intracellular domain of Delta1 results in a non‐proliferating senescent‐like cell phenotype which is dependent on the expression of the cell cycle inhibitor, p21, and is abolished by co‐expression of constitutively active Notch1. These data suggest a new intracellular role for Delta1.