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Thomas McGonigal

Researcher at Abbott Laboratories

Publications -  10
Citations -  1425

Thomas McGonigal is an academic researcher from Abbott Laboratories. The author has contributed to research in topics: Protein kinase B & Cancer cell. The author has an hindex of 9, co-authored 10 publications receiving 1345 citations.

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Potent and selective inhibitors of Akt kinases slow the progress of tumors in vivo.

TL;DR: The development of a series of potent and selective indazole-pyridine based Akt inhibitors is reported, which inhibit Akt-dependent signal transduction in cells and in vivo in a dose-responsive manner and slow the progression of tumors when used as monotherapy or in combination with paclitaxel or rapamycin.
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Survivin enhances Aurora-B kinase activity and localizes Aurora-B in human cells.

TL;DR: It is demonstrated that in the presence ofsurvivin, Aurora-B phosphorylates histone H3 much more efficiently than in the absence of survivin in a cell-free system, thus providing a mechanism as to how survivin exerts its function in human cells.
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Phenotype in Candida albicans of a disruption of the BGL2 gene encoding a 1,3-beta-glucosyltransferase.

TL;DR: Loss of Bgl2p function renders cells more dependent on chitin for wall integrity, and attenuates virulence (probably due to subtle changes in wall structure), and indicates that additional 1,3-beta-glucosyltransferases are present in the C. albicans BGL2 disruptant.
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Acquired resistance to combination treatment with temozolomide and ABT-888 is mediated by both base excision repair and homologous recombination DNA repair pathways.

TL;DR: It is suggested that cancer cells upregulate the homologous recombination DNA repair pathway to compensate for the loss of base excision repair, which may account for the observed resistance to treatment with TMZ and ABT-888.