Department of Neuroscience, UF Scripps Biomedical Research, Jupiter, FL, USA.
Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, HBNI, Kolkata, India.
Methods Mol Biol. 2024;2761:267-276. doi: 10.1007/978-1-0716-3662-6_19.
Cytoskeletal and microtubule atrophy are major hallmarks of Alzheimer's disease (AD). A method to investigate endogenous proteins that can interact/stabilize the cytoskeleton (under pathological cues) is rare. Here, we describe how receptor tyrosine kinase-like orphan receptor 1 (ROR1), a receptor tyrosine kinase (RTK), can act as a neuroprotective molecule by promoting neurite outgrowth, stabilizing cytoskeletal components, and altering the dynamics of actin assembly in a cell culture model of AD.
细胞骨架和微管萎缩是阿尔茨海默病 (AD) 的主要特征。一种研究可以与细胞骨架相互作用/稳定细胞骨架(在病理提示下)的内源性蛋白质的方法很少见。在这里,我们描述了受体酪氨酸激酶样孤儿受体 1 (ROR1) 如何作为一种神经保护分子发挥作用,通过促进神经突生长、稳定细胞骨架成分以及改变 AD 细胞培养模型中肌动蛋白组装的动力学来实现。