mProX™ Human PAK1 Stable Cell Line

Bu, Fan. et al. "Activation of cerebral Ras-related C3 botulinum toxin substrate (Rac) 1 promotes post-ischemic stroke functional recovery in aged mice." Neural regeneration research, 2024.
After a stroke, individuals commonly experience brain functional impairment, yet the specific molecular mechanisms of post-stroke recovery are not well understood. Research has shown that advanced age is a significant predictor of poor outcomes, particularly in terms of functional recovery, after a stroke. Studies have suggested that axonal regeneration and angiogenesis, two important forms of brain plasticity, are reduced in older individuals. However, previous research has shown that activating Ras-related C3 botulinum toxin substrate (Rac) 1 can improve recovery in younger mice models. To further explore this, a team investigated the role of Rac1 signaling in long-term functional recovery and brain plasticity in aged male C57BL/6J mice (18 to 22 months old) after ischemic stroke. The team found that Rac1 expression decreased with aging and that delayed overexpression of Rac1 improved cognitive and sensorimotor recovery in the aged mice. Immunostaining also showed an increase of neurite (nerve cell extension) and proliferative endothelial cells (cells that make up blood vessels) in the peri-infarct zone (area surrounding the damaged brain tissue). In contrast, inhibiting Rac1 using a pharmacological agent worsened the outcome, decreasing the number of neurites and proliferative endothelial cells. This approach also reduced the activation of p21-activated kinase 1 (a protein involved in cell movement and adhesion), decreased the protein level of brain-derived neurotrophic factor (a protein that helps promote nerve cell survival and growth), and increased the protein level of glial fibrillary acidic protein (a protein found in astrocytes, a type of brain cell). This study sheds light on the mechanisms underlying decreased plasticity after stroke in aging brains and suggests that targeting Rac1 may be a potential therapeutic strategy for improving recovery in older adults after a stroke. These findings were published in the Journal of Aging and Stroke.
Bu, Fan. et al. "Activation of cerebral Ras-related C3 botulinum toxin substrate (Rac) 1 promotes post-ischemic stroke functional recovery in aged mice." Neural regeneration research, 2024.
Pubmed: 37843224   DOI: 10.4103/1673-5374.382256

Feng, Xing et al. "Hypoxia-induced acetylation of PAK1 enhances autophagy and promotes brain tumorigenesis via phosphorylating ATG5." Autophagy vol. 17,3 (2021): 723-742.
In the investigation of brain tumor treatment through the regulation of kinase-controlled macroautophagy, the specific mechanism governing autophagy initiation and its importance in glioblastoma (GBM) remains undefined. This study reveals a significant upregulation of PAK1 (p21 [RAC1] activated kinase 1) that promotes GBM development, particularly associated with autophagy, according to Cancer Genome Atlas analysis. Experiments further establish PAK1 as a positive modulator for hypoxia-induced autophagy in GBM, driven by ELP3-mediated acetylation at K420. This modification enhances PAK1 activity, leading to ATG5 phosphorylation at T101, thus facilitating autophagosome formation and GBM tumorigenesis. Silencing PAK1 inhibits autophagy and GBM growth, while SIRT1-mediated PAK1-deacetylation hinders both. Clinically, PAK1 acetylation at K420 significantly correlates with ATG5 phosphorylation at T101 in GBM patients, suggesting potential therapeutic targets for GBM treatment.
Feng, Xing et al. "Hypoxia-induced acetylation of PAK1 enhances autophagy and promotes brain tumorigenesis via phosphorylating ATG5." Autophagy vol. 17,3 (2021): 723-742.
Pubmed: 32186433   DOI: 10.1080/15548627.2020.1731266