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Andrew Burgess

Researcher at University of Sydney

Publications -  70
Citations -  4726

Andrew Burgess is an academic researcher from University of Sydney. The author has contributed to research in topics: Mitosis & Cell cycle. The author has an hindex of 28, co-authored 69 publications receiving 4192 citations. Previous affiliations of Andrew Burgess include Garvan Institute of Medical Research & University of Queensland.

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Partial inhibition of Cdk1 in G2 phase overrides the SAC and decouples mitotic events

TL;DR: Results show that continuous and subtle disruption of Cdk1 activity from G2 phase onwards has deleterious consequences on mitotic progression by disrupting the balance between Cdk2A and PP2A, which supports the current model thatPP2A is the primary phosphatase that counterbalances the activity of Ckk1 during mitosis.
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Loss of human Greatwall results in G2 arrest and multiple mitotic defects due to deregulation of the cyclin B-Cdc2/PP2A balance

TL;DR: It is shown that the functional human ortholog of Greatwall protein kinase (Gwl) is the microtubule-associated serine/threonine kinase-like protein, MAST-L, and that Gwl is crucial for mediating this regulation in somatic human cells.
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The Substrate of Greatwall Kinase, Arpp19, Controls Mitosis by Inhibiting Protein Phosphatase 2A

TL;DR: This work describes how Gwl activation results in PP2A inhibition and identifies cyclic adenosine monophosphate–regulated phosphoprotein 19 (Arpp19) and α-Endosulfine as two substrates of Gwl that, when phosphorylated by this kinase, associate with and inhibitPP2A, thus promoting mitotic entry.
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Clinical Overview of MDM2/X-Targeted Therapies

TL;DR: Preclinical modeling, which has demonstrated effective in vitro and in vivo killing of WT p53 cancer cells, has now been translated into early clinical trials allowing better assessment of their biological effects and toxicities in patients.
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Histone Deacetylase Inhibitors Trigger a G2 Checkpoint in Normal Cells That Is Defective in Tumor Cells

TL;DR: It is reported that histone deacetylase inhibitors, in particular azelaic bishydroxamic acid, triggers a G2 phase cell cycle checkpoint response in normal human cells, and this checkpoint is defective in a range of tumor cell lines.