Polo like kinase Plx1 is required for the inhibition of Op18 in extracts of Flt Signaling eggs, but the r M ge Be indirect, because neither Ser 16, Ser 25, Ser 39 or Fit Polo known consensus phosphorylation sites. However, Ser 16 is not good agreement with Aurora kinase consensus sites. Aur B and its counterpart IPL1 yeast are essential for processes that unsachgem S kinetochore microtubules Anh length To l Sen and lead to alignment on the metaphase spindle bipolar sister correct. Aur B is part of a multi-subunit, chromosomal passenger complex, the chromosomes combine w During mitosis at the beginning, in somatic cells, at the centromeres is focused interior. Inhibition of Aur B st rt Localization of several proteins and centromeres kinetochores including normal MCAK. Phosphorylated in vitro and inhibits Aur B MCAK.
Phosphorylation of MCAK localized centromere Aur B is assumed that MCAK, microtubules s more target depolymerization activity t in the N Height of the kinetochores block, suggesting that cycles of phosphorylation and dephosphorylation of MCAK important for stabilizing microtubules, kinetochores and fixation which accompany the right direction bipolar sister. Aur ZD4054 A is necessary for the maintenance and development of the bipolar spindle and in many cells. W During mitosis Aur A at centrosomes and spindle microtubules N He concentrates. Phosphorylation of Aur within the activation loop for their T Ben activity CONFIRMS. Inhibitory signals from the mitotic chromosomes increased greatly Hen the activity t of Aur A.
W During mitosis, chromatin generated YEARS Ring guanine nucleotide exchange factor RCC1 one Erh Increase the local concentration of Ran GTP, shifting factor TPX2 spindle assembly Association importins. Interaction with TPX2 Aur A erh Ht his Kinaseaktivit t. Thus, it is possible to change that a small population of active Aur A near mitotic chromosomes, where they participate in the regulation of microtubule interactions with chromosomes can k Are. With Xenopus extracts of eggs, we find that the Aurora kinase inhibitor ZM447439 Bl press Hyperphosphorylation of chromatin-induced Op18 previously with inhibition Op18 localized N He associated chromosomes. AlthoughZM was regarded as a highly selective inhibitor of Aur B cells, we find that ZM blocked the phosphorylation of Aur A activation loop Thr 295th Immunodepletions show Aur A which is necessary for the onset of nucleation induced microtubule centrosome is not essential either for the subsequent formation of organized bipolar spindles.
To mitotic chromatin or hyperphosphorylation Op18 Depletion of Aur B Bl Cke. Spindle both the capacity t And induce mitotic chromatin to Op18 hyperphosphorylation These results support current That r next to his In the regulation of the activity of MCAK t Aur B inhibiting localized Op18 w During spindle required. As a result, ZM erm glicht Ersch Pfungstadt Aur B aster formation, but the following Bl cke chromosomal spindle Organizes Training: Depletion of Aur A st formation Aster spindle formation but not rt ter sp.