ReviewExperimental & molecular medicine2026
PAK4 in metabolic diseases: regulation by nutrient signals and therapeutic implications.
Review in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- p21-activated kinase 4 drives hepatic stellate cell activation and liver fibrosis through the phosphorylation of YAP at T428.Signal transduction and targeted therapy · 2026Article
- Phosphoproteomic Profiling Identifies PAK4 S474 Phosphorylation Affects Docetaxel Chemosensitivity via Modulation of Microtubule Stabilization in Breast Cancer.Biomedicines · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here we highlight recent advances in understanding the regulatory role of p21-activated kinase 4 (PAK4), the prototypical group II PAK family member, in metabolic diseases. It also briefly notes the contributions of the group I member PAK1 in metabolic tissues. Activation of PAK4 is mediated by upstream Ras-related small GTPases such as Cdc42 and Rac1. In addition to this classical mechanism, post-translational modifications triggered by growth factors and hormonal signals are now recognized as key determinants of PAK4 activity and expression. Notably, phosphorylation-dependent ubiquitination followed by proteasomal degradation-initiated by changes in cellular energy availability-has emerged as an important mechanism regulating PAK4 protein stability. PAK4, in turn, phosphorylates a broad range of intracellular signaling proteins and transcriptional regulators, thereby orchestrating communication among the liver, adipose tissue and skeletal muscle. Accumulating evidence indicates that aberrant overexpression of PAK4 contributes to the progression of metabolic diseases, whereas reduced PAK4 activity may provide protective benefits. These insights collectively support the therapeutic potential of targeting PAK4 in obesity, type 2 diabetes and metabolic dysfunction-associated steatotic liver disease. Moreover, recognition of PAK4's kinase-independent scaffold functions has stimulated the development of PAK4-targeted protein degraders, expanding therapeutic opportunities.
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