• In 1997, RAD21 was independently discovered by two groups to be a major component of the chromosomal cohesin complex, and its dissolution by the cysteine protease Separase at the metaphase to anaphase transition results in the separation of sister chromatids and chromosomal segregation. (wikipedia.org)
  • The acquiring that separase is overexpressed in many cancers, including CML renders this protease a essential subject of investigation to unravel the molecular mechanisms involved with the growth of centrosome amplification in IM handled CML. (pkc-inhibitors.com)
  • Separase proteolytic activity is tightly regulated by a number of inhibitory mechanisms combining Securin binding, JAK phosphorylation precise serine residue phosphorylation by CyclinB1 Cdk1, PP2A binding and autocatalytic cleavage. (pkc-inhibitors.com)
  • Ectopic activation of Separase proteolytic activity brings about premature sister chromatide separation and centriole disengagement. (pkc-inhibitors.com)
  • ESPL1 / separase, a cysteine ​​endopeptidase, is a key player in centrosome duplication and mitotic sister chromatid separation. (separase.com)
  • We report on separase transcription, protein expression, and Separase proteolytic activity. (pkc-inhibitors.com)
  • We observed a publish translational activation of Separase proteolytic activity in BCR ABL positive cells soon after treatment method with therapeutic IM doses. (pkc-inhibitors.com)
  • Effects Study style and cell line characterization To analyze the conditional context in between p210BCR ABL, separase activity and IM remedy, we carried out cell culture experiments applying a panel of six nicely established human cell lines. (pkc-inhibitors.com)
  • Increased separase activity and occurrence of centrosome aberrations concur with transformation of MDS. (separase.com)
  • Sepin-1 is a small compound that inhibits the enzymatic activity of Separase and growth of cancer cells. (separase.com)
  • Separase activity distribution can be a marker of major molecular response and proliferation of CD34+ cells in TKI-treated chronic myeloid leukemia patients. (separase.com)