@article {761,
	title = {Monitoring developmental force distributions in reconstituted embryonic epithelia.},
	journal = {Methods},
	year = {2015},
	month = {2015 Sep 2},
	abstract = {<p>The way cells are organized within a tissue dictates how they sense and respond to extracellular signals, as cues are received and interpreted based on expression and organization of receptors, downstream signaling proteins, and transcription factors. Part of this microenvironmental context is the result of forces acting on the cell, including forces from other cells or from the cellular substrate or basement membrane. However, measuring forces exerted on and by cells is difficult, particularly in an in vivo context, and interpreting how forces affect downstream cellular processes poses an even greater challenge. Here, we present a simple method for monitoring and analyzing forces generated from cell collectives. We demonstrate the ability to generate traction force data from human embryonic stem cells grown in large organized epithelial sheets to determine the magnitude and organization of cell-ECM and cell-cell forces within a self-renewing colony. We show that this method can be used to measure forces in a dynamic hESC system and demonstrate the ability to map intracolony protein localization to force organization.</p>
},
	issn = {1095-9130},
	doi = {10.1016/j.ymeth.2015.09.003},
	author = {Przybyla, L and Lakins, J N and Sunyer, R and Trepat, X and Weaver, V M}
}
@article {256,
	title = {Oncogenic targeting of BRM drives malignancy through C/EBPβ-dependent induction of α5 integrin.},
	journal = {Oncogene},
	year = {2013},
	month = {2013 Jun 17},
	abstract = {<p>Integrin expression and activity are altered in tumors, and aberrant integrin signaling promotes malignancy. However, how integrins become altered in tumors remains poorly understood. We discovered that oncogenic activation of MEK signaling induces cell growth and survival, and promotes the malignant phenotype of mammary epithelial cells (MECs) by increasing α5 integrin expression. We determined that MEK activates c-Myc to reduce the transcription of the SWI/SNF chromatin remodeling enzyme Brahma (BRM). Our studies revealed that reduced BRM expression and/or activity drives the malignant behavior of MECs by epigenetically promoting C/EBPβ expression to directly induce α5 integrin transcription. Consistently, we could show that restoring BRM levels normalized the malignant behavior of transformed MECs in culture and in vivo by preventing C/EBPβ-dependent α5 integrin transcription. Our findings identify a novel mechanism whereby oncogenic signaling promotes malignant transformation by regulating transcription of a key chromatin remodeling molecule that regulates integrin-dependent stromal-epithelial interactions.Oncogene advance online publication, 17 June 2013; doi:10.1038/onc.2013.220.</p>
},
	issn = {1476-5594},
	doi = {10.1038/onc.2013.220},
	author = {Damiano, L and Stewart, K M and Cohet, N and Mouw, J K and Lakins, J N and Debnath, J and Reisman, D and Nickerson, J A and Imbalzano, A N and Weaver, V M}
}
