A Cell Biologist's Field Guide to Aurora Kinase Inhibitors.
Los Angeles, United States. In Front Oncol, 2014
In a cellular context, we demonstrate that immunofluorescence-based detection of LATS2 and histone H3 phospho-epitopes provides a facile and reliable means to assess potency and specificity of Aurora A versus Aurora B inhibition, and that G2 duration measured in a live imaging assay is a specific readout of Aurora A activity.
Role of microRNA-93 in regulation of angiogenesis.
Tianjin, China. In Tumour Biol, 2014
MiRNA-93's effects on angiogenesis are dependent on the interaction of other multiple genes and signal pathways, such as P21, E2F1, integrin-β8, LATS2, etc. Future investigation should involve mapping the network by which miRNA-93 exerts its functions.
Hippo pathway key to ploidy checkpoint.
Hangzhou, China. In Cell, 2014
report that extra centrosome-induced activation of the Hippo pathway kinase LATS2 is a key mechanism of tetraploidy-induced cell-cycle arrest.
An emerging role for Hippo-YAP signaling in cardiovascular development.
Augusta, United States. In J Biomed Res, 2014
Recent studies demonstrate that cardiac-specific deletion of the Hippo pathway kinase Mst (STE20-like protein kinases) co-activator WW45 (WW domain-containing adaptor 45), Mst1, Mst2, or Lats2 (large tumor suppressor homologue 2) in mice result in over-grown hearts with elevated cardiomyocyte proliferation.
Function and cancer genomics of FAT family genes (review).
Tokyo, Japan. In Int J Oncol, 2012
Copy number aberration, translocation and point mutation of FAT1, FAT2, FAT3, FAT4, FRMD1, FRMD6, NF2, WWC1, WWC2, SAV1, STK3, STK4, MOB1A, MOB1B, LATS1, LATS2, YAP1 and WWTR1/TAZ genes should be comprehensively investigated in various types of human cancers to elucidate the mutation landscape of the FAT‑Hippo signaling cascades.
p53: guardian of ploidy.
Portugal. In Mol Oncol, 2011
The tumor suppressor Lats2, along with other tumor inhibitory proteins such as BRCA1/2 and BubR1, are central to p53-dependent elimination of tetraploid cells.
Mst out and HCC in.
San Diego, United States. In Cancer Cell, 2009
Unexpectedly, Mst1/2 may activate another kinase besides Lats1 and Lats2 to phosphorylate YAP, and the role of Mst1/2 in YAP regulation is cell type dependent.