Restoration treatments enhance tree growth and alter climatic constraints during extreme drought.

The frequency and severity of drought events are predicted to increase due to anthropogenic climate change, with cascading effects across forested ecosystems. Management activities such as forest thinning and prescribed burning, which are often intended to mitigate fire hazard and restore ecosystem processes, may also help promote tree resistance to drought. However, it is unclear whether these treatments remain effective during the most severe drought conditions or whether their impacts differ across environmental gradients.

Nuclear Focal Adhesion Kinase Protects against Cisplatin Stress in Ovarian Carcinoma.

FAK inhibitors are in combinatorial clinical testing with agents that prevent Ras-Raf-MAPK pathway activation in various cancers. This study suggests that nuclear FAK limits ERK/MAPK activation in supporting HGSOC cell survival to cisplatin stress. Overall, it is likely that targets of FAK-mediated survival signaling may be tumor type- and context-dependent.

Declining ecological resilience and invasion resistance under climate change in the sagebrush region, United States.

In water-limited dryland ecosystems of the Western United States, climate change is intensifying the impacts of heat, drought, and wildfire. Disturbances often lead to increased abundance of invasive species, in part, because dryland restoration and rehabilitation are inhibited by limited moisture and infrequent plant recruitment events. Information on ecological resilience to disturbance (recovery potential) and resistance to invasive species can aid in addressing these challenges by informing long-term restoration and conservation planning.

Inducible FAK Deletion but not FAK Inhibition in Endothelial Cells Activates p53 to Suppress Tumor Growth in PYK2-null Mice.

Unlabelled: Focal adhesion kinase (FAK) functions as a signaling and scaffolding protein within endothelial cells (ECs) impacting blood vessel function and tumor growth. Interpretations of EC FAK-null phenotypes are complicated by related PYK2 (protein tyrosine kinase 2) expression, and to test this, we created PYK2 FAK mice with tamoxifen-inducible EC-specific Cre recombinase expression. At 11 weeks of age, EC FAK inactivation resulted in increased heart and lung mass and vascular leakage only on a PYK2 background.

Focal adhesion kinase signaling - tumor vulnerabilities and clinical opportunities.

Focal adhesion kinase (FAK; encoded by PTK2) was discovered over 30 years ago as a cytoplasmic protein tyrosine kinase that is localized to cell adhesion sites, where it is activated by integrin receptor binding to extracellular matrix proteins. FAK is ubiquitously expressed and functions as a signaling scaffold for a variety of proteins at adhesions and in the cell cytoplasm, and with transcription factors in the nucleus. FAK expression and intrinsic activity are essential for mouse development, with molecular connections to cell motility, cell survival and gene expression.