The combination of molecular imaging, genetic and pharmacological approaches revealed that BCR signaling and PKCβ-dependent activation of focal adhesion kinase (FAK) is required for B cell mechanosensing.
Disrupting extrusion, a process that drives epithelial cell death, leads to increased cell survival, poor barrier function, and enhanced cell invasion and, thereby, promotes tumor initiation and progression.
Integrin a11 is identified as an Osteolectin receptor, revealing a new mechanism for adult skeletal bone maintenance in which Osteolectin/a11b1 signaling promotes bone formation by activating the Wnt pathway.
An unprecedented large-scale screen in mice for morphogenetic regulators of tissue development provides major new insights into the roles of Rho GTPases in diverse array of skin developmental processes.
Genomic gains in ovarian cancer can promote cisplatin resistance via a FAK, Wnt/beta-catenin and Myc signaling pathway supporting pluripotency genes and tumorspheres that can acquire FAK dependence for survival.
Integrin and actin associated proteins are resolved into four layers within myofibril attachments, an architecture requiring balanced positive and negative regulation of integrin adhesion with integrated mechanotransduction and actin pathways.
Cancer cell expression of the T-cell co-stimulatory molecule CD80, or treatment with agonistic antibodies targeting the T-cell co-stimulatory receptors OX-40 or 4-1BB, enhances the anti-tumor activity of FAK inhibition.