Imputation of Quantitative Genetic Interactions in Epistatic MAPs by Interaction Propagation Matrix Completion

Author(s):  
Marinka Žitnik ◽  
Blaž Zupan
Cell ◽  
2010 ◽  
Vol 141 (5) ◽  
pp. 739-745 ◽  
Author(s):  
Pedro Beltrao ◽  
Gerard Cagney ◽  
Nevan J. Krogan

PLoS ONE ◽  
2008 ◽  
Vol 3 (9) ◽  
pp. e3284 ◽  
Author(s):  
Aki P. Järvinen ◽  
Jukka Hiissa ◽  
Laura L. Elo ◽  
Tero Aittokallio

Author(s):  
Colm Ryan ◽  
Gerard Cagney ◽  
Nevan Krogan ◽  
Pádraig Cunningham ◽  
Derek Greene

2009 ◽  
Vol 10 (12) ◽  
pp. R140 ◽  
Author(s):  
Igor Ulitsky ◽  
Nevan J Krogan ◽  
Ron Shamir

2020 ◽  
Author(s):  
Patricia Pascual-Vargas ◽  
Mar Arias-Garcia ◽  
Theodoros I. Roumeliotis ◽  
Jyoti S. Choudhary ◽  
Chris Bakal

AbstractYAP and TAZ are transcriptional co-activators that are often constitutively active in triple negative breast cancer (TNBC) cells driving proliferation, invasion, and drug resistance. Through multiplexed quantitative genetic screens for YAP/TAZ localisation and cell shape, we found that the RhoGEF DOCK5 is essential for YAP/TAZ activation in metastatic cells and is required for the maintenance of polarity during migration. DOCK5 regulates cell shape and thus YAP/TAZ through different genetic interactions with CDC42, RAC, and RHOA GTPases. DOCK5 regulates focal adhesion (FA) morphogenesis in RAC-dependent fashions that promote RHOA mediated actomyosin engagement of FA. Using unbiased systems-level quantification of protein levels by mass spectrometry we show that DOCK5 maintains polarity by stabilising protein levels of the CDC42 effector GSK3β. We conclude DOCK5 acts as a coincidence detector to promote leading edge persistence in subcellular locations where there is both RAC and RHOA dependent FA morphogenesis and active CDC42 mediated cell polarisation.


2008 ◽  
Vol 4 (1) ◽  
pp. 209 ◽  
Author(s):  
Igor Ulitsky ◽  
Tomer Shlomi ◽  
Martin Kupiec ◽  
Ron Shamir

2014 ◽  
Author(s):  
Miao Fan ◽  
Deli Zhao ◽  
Qiang Zhou ◽  
Zhiyuan Liu ◽  
Thomas Fang Zheng ◽  
...  

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