Aurora kinase A (AURKA), a known transcriptional target of FoxM1 (Lefebvre et al., 2010), was used as a positive control.
Given this observation, we hope that the off - target effects on
Aurora kinase B and ERBB2 (if any) will also be in a vastly different concentration range of 100 nM.
A low, non-genotoxic, dose (about 1 nM) of ActD has been shown to induce a reversible cytostatic effect in normal proliferating dermal fibroblasts and protect them from the aneuploidy induced by
the aurora kinase inhibitor VX - 680 and the toxic effects of gemcitabine [46, 47].
Many of these kinases are involved in growth - related pathways, tumorigenesis pathways, and cell cycle control, such as
Aurora kinase B (Borisa and Bhatt, 2017).
A comprehensive review on
Aurora kinase: small molecule inhibitors and clinical trial studies
Rao B, van Leeuwen IM, Higgins M, Campbel J, Thompson AM, Lane DP and Lain S. Evaluation of an Actinomycin D / VX -680
aurora kinase inhibitor combination in p53 - based cyclotherapy.
The first trial to take place as a result of the CDP initiative is a Phase I clinical trial of GlaxoSmithKline's
aurora kinase inhibitor GSK - 1070916A - a promising new drug to treat solid tumours.
In a discovery screen profiling 102 cell lines against 8,400 compounds, PRISM led the researchers to a specific novel compound, BRD - 7880; the specific action against cell lines in the panel rapidly led them to discover that this compound worked by inhibiting
aurora kinase B, an enzyme involved in cell division that is abnormally regulated in several cancers.
Short and long - term tumor cell responses to
Aurora kinase inhibitors.
KIBRA regulates
Aurora kinase activity and is required for precise chromosome alignment during mitosis % U http://www.jbc.org/content/early/2012/08/17/jbc.M112.385518.short.
KIBRA regulates
Aurora kinase activity and is required for precise chromosome alignment during mitosis.
Now drugs that inhibit
aurora kinase A are in clinical trials for several types of cancer, and clinicans are planning to examine whether the same type of drugs could help with graft - vs - host disease.
Winship Cancer Instituteâ $ ™ s Ned Waller and researchers from Childrenâ $ ™ s Healthcare of Atlanta and Yerkes National Primate Research Center were part of a recent Science Translational Medicine paper that draws a bright red circle around
aurora kinase A as a likely drug target in graft - vs - host disease.
The pathway Kean and her team studied is
Aurora Kinase A, a well - known genetic target for cancer researchers.
The drug inhibits
the Aurora Kinase A signaling pathway, causing cells to stop dividing.
Aurora kinase has many subtypes, but is generally known for its role in cell division — an additional link between regeneration and division that helped to confirm Lin was on to something.
These tests revealed that an enzyme called
Aurora kinase plays a key role in Stentor regeneration.
Lin also found that inhibiting a different type of
Aurora kinase completely suppressed Stentor's regeneration.
Our results suggest that frequent overexpression of
Aurora Kinase in cancer may reduce RUNX3 transcription activity, leading to cell division and formation of tumours.
Understanding the molecular mechanisms underlying
Aurora kinase - overexpressing tumours will help in the design of targeted and personalised cancer therapy,» said Dr Linda Chuang, Senior Research Scientist at CSI Singapore, who is the first author of the study.
She then discovered that if she inhibited one of
the Aurora kinases, it actually sped up regeneration in Stentor.
Aurora kinases are enzymes that control mitosis, the process of cell division, and were first discovered in the 1990s in yeast, flies and frogs.
This expression pattern of MELK, which is similar to that of Cyclin B1 and
Aurora kinases, indicates that MELK is a mitotic kinase in BBC cells.
Not exact matches
Histone H3 is specifically phosphorylated, presumably by the oncogenic
kinase Aurora B, at serine 10 at the onset of mitosis.