Publications by authors named "F A Kruyt"

Article Synopsis
  • Microglia are the brain's key immune cells, interacting with neurons and other glial cells, crucial for maintaining brain function, and their disruption can lead to neurodegenerative diseases like Alzheimer's and Parkinson's.
  • Access to actual human brain tissue is limited, making it challenging to study microglia's role in disease; however, advancements in pluripotent stem cell technology have allowed researchers to create complex models for this purpose.
  • Recent developments in brain organoids, which simulate the brain's 3D environment and cellular interactions, are providing new insights into microglial functioning and their potential to investigate various brain pathologies.
View Article and Find Full Text PDF

Stiffening of the brain extracellular matrix (ECM) in glioblastoma promotes tumor progression. Previously, we discovered that protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) plays a role in glioblastoma stem cell (GSC) adaptation to matrix stiffness through PERK/FLNA-dependent F-actin remodeling. Here, we examined the involvement of PERK in detecting stiffness changes via focal adhesion complex (FAC) formation.

View Article and Find Full Text PDF

Objective: Meningiomas are one of the most frequently occurring brain tumors and can be curatively treated with gross-total resection. A subtotal resection increases the chances of recurrence. The intraoperative identification of invisible tumor remnants by using a fluorescent tracer targeting an upregulated biomarker could help to optimize meningioma resection.

View Article and Find Full Text PDF

The therapeutic targeting of the tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) death receptors in cancer, including non-small cell lung cancer (NSCLC), is a widely studied approach for tumor selective apoptotic cell death therapy. However, apoptosis resistance is often encountered. The main aim of this study was to investigate the apoptotic mechanism underlying TRAIL sensitivity in three bortezomib (BTZ)-resistant NSCLC variants, combining induction of both the intrinsic and extrinsic pathways.

View Article and Find Full Text PDF