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Securin is required for chromosomal stability in human cells.

Abnormalities of chromosome number are the most common genetic aberrations in cancer. The mechanisms regulating the fidelity of mitotic chromosome transmission in mammalian cells are therefore of great interest. Here we show that human cells without an hSecurin gene lose chromosomes at a high frequency. This loss was linked to abnormal anaphases during which cells underwent repetitive unsuccessful attempts to segregate their chromosomes. The abnormal mitoses were associated with biochemical defects in the activation of separin, the sister-separating protease, rendering it unable to cleave the cohesin subunit Scc1 efficiently. These results illuminate the function of mammalian securin and show that it is essential for the maintenance of euploidy.

Pubmed ID: 11371342

Authors

  • Jallepalli PV
  • Waizenegger IC
  • Bunz F
  • Langer S
  • Speicher MR
  • Peters JM
  • Kinzler KW
  • Vogelstein B
  • Lengauer C

Journal

Cell

Publication Data

May 18, 2001

Associated Grants

  • Agency: NCI NIH HHS, Id: CA 43460
  • Agency: NCI NIH HHS, Id: CA 57345
  • Agency: NCI NIH HHS, Id: CA 62924
  • Agency: NIGMS NIH HHS, Id: GM 41690
  • Agency: NIGMS NIH HHS, Id: GM07309

Mesh Terms

  • Amino Acid Sequence
  • Anaphase
  • Cell Cycle Proteins
  • Centromere
  • Chromosomal Proteins, Non-Histone
  • Chromosome Aberrations
  • Chromosome Disorders
  • Chromosomes, Human
  • Gene Deletion
  • HeLa Cells
  • Humans
  • Molecular Sequence Data
  • Mutagenesis
  • Nuclear Proteins
  • Phosphoproteins
  • Saccharomyces cerevisiae Proteins
  • Sister Chromatid Exchange
  • Spindle Apparatus