| Cat.No. | Product Name | Price |
|---|---|---|
| CLKO-0183 | PKN2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-0185 | PAK2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-1758 | PKN2 KO Cell Lysate-HCT116 | Inquiry |
| CSC-DC011262 | Panoply™ Human PAK2 Knockdown Stable Cell Line | Inquiry |
| CSC-DC011850 | Panoply™ Human PKN2 Knockdown Stable Cell Line | Inquiry |
| CSC-RT0677 | Human PKN2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT0679 | Human PAK2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT1903 | PKN2 Knockout Cell Line-HCT116 | Inquiry |
| CSC-SC011262 | Panoply™ Human PAK2 Over-expressing Stable Cell Line | Inquiry |
| CSC-SC011850 | Panoply™ Human PKN2 Over-expressing Stable Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CLKO-0183 | PKN2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-0185 | PAK2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-1758 | PKN2 KO Cell Lysate-HCT116 | Inquiry |
| CSC-DC011262 | Panoply™ Human PAK2 Knockdown Stable Cell Line | Inquiry |
| CSC-DC011850 | Panoply™ Human PKN2 Knockdown Stable Cell Line | Inquiry |
| CSC-RT0677 | Human PKN2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT0679 | Human PAK2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT1903 | PKN2 Knockout Cell Line-HCT116 | Inquiry |
| CSC-SC011262 | Panoply™ Human PAK2 Over-expressing Stable Cell Line | Inquiry |
| CSC-SC011850 | Panoply™ Human PKN2 Over-expressing Stable Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CLKO-0183 | PKN2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-0185 | PAK2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-1758 | PKN2 KO Cell Lysate-HCT116 | Inquiry |
| CSC-DC011262 | Panoply™ Human PAK2 Knockdown Stable Cell Line | Inquiry |
| CSC-DC011850 | Panoply™ Human PKN2 Knockdown Stable Cell Line | Inquiry |
| CSC-RT0677 | Human PKN2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT0679 | Human PAK2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT1903 | PKN2 Knockout Cell Line-HCT116 | Inquiry |
| CSC-SC011262 | Panoply™ Human PAK2 Over-expressing Stable Cell Line | Inquiry |
| CSC-SC011850 | Panoply™ Human PKN2 Over-expressing Stable Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CLKO-0183 | PKN2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-0185 | PAK2 KO Cell Lysate-HeLa | Inquiry |
| CLKO-1758 | PKN2 KO Cell Lysate-HCT116 | Inquiry |
| CSC-DC011262 | Panoply™ Human PAK2 Knockdown Stable Cell Line | Inquiry |
| CSC-DC011850 | Panoply™ Human PKN2 Knockdown Stable Cell Line | Inquiry |
| CSC-RT0677 | Human PKN2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT0679 | Human PAK2 Knockout Cell Line-HeLa | Inquiry |
| CSC-RT1903 | PKN2 Knockout Cell Line-HCT116 | Inquiry |
| CSC-SC011262 | Panoply™ Human PAK2 Over-expressing Stable Cell Line | Inquiry |
| CSC-SC011850 | Panoply™ Human PKN2 Over-expressing Stable Cell Line | Inquiry |
Functional dichotomy of Pak2, which is serine/threonine kinase as a member if the group I Pak family, in cell survival has been described in previous studies. Activation of full-length Pak2 is cell survival stimulative, whereas the caspase3-cleaved short form, Pak-p34, promoted cell death. Pro-survival role for Pak2 was firstly evidenced by zebrafish models, where autonomous endothelial cell defects and hemorrhage occurred after removal of Pak2. Global deletion of Pak2 culminated in embryonic demise while endothelial specific deletion gave rise to the flawed blood vessel formation, all of which suggests the indispensable role of Pak2 in endothelial cell survival and angiogenesis.
As a stress-responsive kinase with localization of close proximity to ER membrane in cardiomyocytes, pak2 can activate Rac1/Cdc42 signaling pathway. A Pak2 promoted protective ER stress response under ER stress conditions was revealed by the phenotypic analysis in cardiac Pak2 knockout mice. Mechanistic study of gene array data demonstrated that Pak2 regulated ER function protection is IRE1/XBP1 pathway dependent. This was further corroborated by IRE activator that relieved ER dysfunction in Pak2-CKO hearts. Hearts injured from CVD (cardiovascular disease), which is still ranked as the leading cause of death worldwide, eventually progress to heart failure (HF), the cause of which is massive cardiomyocyte loss in despite of numerous causative factors. Vulnerability of cardiomyocytes to ER stress is the consequence of their poor regenerative capacity and dependence on trans-membrane proteins, such as ion channels for contractile processes. Oxidative stress, energy deprivation, abnormal calcium content and inflammation, all of which can role as disruptive factors for ER folding and ER stress inducer.
In neurodevelopmental disorders, such as autism spectrum disorder (ASD), synaptic cytoskeleton dysfunction is always represented as a common pathogenesis. As a critical regulator of cytoskeleton dynamics, serine/threonine kinase Pak2 was found to be functional in central nervous system and ASD pathogenesis. Pak2 haploinsufficiency gave the consequence of markedly decreased synapse densities, defective long-term potentiation, and autism-related behaviors in mice. Functional networks related to ASD are perturbed by PAK2 deficiency via actin cytoskeleton dynamics regulation.
Figure 1. The mechanism of PAK2 regulating glucose uptake and insulin sensitivity in neuronal cells. (Pallavi Varshney, et al. 2016)
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