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Human polo-like kinases (PLK1 PLK4) have been implicated in mitotic regulation and carcinogenesis.
In addition to microtubules, stress fibers have recently been implicated in mitotic spindle positioning [38].
CG14781 has been implicated in mitotic spindle elongation and recently shown to correspond to mei-38 [23], [23].
Humans have three different cdc25 proteins, cdc25A, B and C and all have been implicated in mitotic activation [8] [11, respectively].
Many proteins have been implicated in mitotic PCM assembly.
PR-SET7-mediated histone 4 lysine 20 methylation has been implicated in mitotic condensation, DNA damage response and replication licensing.
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In addition, various protein kinases such as Cdc2, polo and aurora and related protein phosphatases are implicated in mitotic control.
Human hCDC14A was proposed to exert its function at centrosome duplication [ 8] while hCDC14B was implicated in mitotic progression [ 9], DNA damage checkpoint activation and DNA repair [ 10].
p53 and its target genes, Bax and PUMA, have been implicated in driving mitotic catastrophe.
For example, highly conserved (from yeast to mammals and plants) PUF proteins have been implicated in maintaining mitotic proliferation and the self-renewal of GSCs [ 32, 33].
As Caspase-2 has been implicated in mediating mitotic catastrophe as a response to DNA-damage after failed cell cycle arrest and that c-Myc overexpression drives proliferation stress leading to DNA damage, we investigated if lack of Caspase-2 would influence genomic stability of normal, premalignant or transformed cells.
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