ArticlePloS one2015
The Cdc42 Effector Kinase PAK4 Localizes to Cell-Cell Junctions and Contributes to Establishing Cell Polarity.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- A complex of MAST1 and 14-3-3η regulates Tau phosphorylation in the developing cortex.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cytoskeletal dynamics in breast cancer: mechanistic insights and therapeutic opportunities.Journal of the National Cancer Center · 2026Review
- PAK4 promotes vertex remodeling to maintain epithelial integrity and barrier function.bioRxiv : the preprint server for biology · 2025Article
- β2-Adrenergic receptor regulates osteoblast differentiation and migration and C-terminal β-catenin phosphorylation.Biochemical and biophysical research communications · 2025Article
- Retinoic acid induced specific changes in the phosphoproteome of C17.2 neural stem cells.Journal of cellular and molecular medicine · 2024Article
- Rho family GTPase signaling through type II p21-activated kinases.Cellular and molecular life sciences : CMLS · 2022Review
- Structure-based design of CDC42 effector interaction inhibitors for the treatment of cancer.Cell reports · 2022Article
- Proximity proteomics identifies PAK4 as a component of Afadin-Nectin junctions.Nature communications · 2021Article
- Rac1-PAK1 regulation of Rab11 cycling promotes junction destabilization.The Journal of cell biology · 2021Article
- Loss of p21-activated kinase Mbt/PAK4 causes Parkinson-like phenotypes in Drosophila.Disease models & mechanisms · 2021Article
- Group II p21-activated kinase, PAK4, is needed for activation of focal adhesion kinases, MAPK, GSK3, and β-catenin in rat pancreatic acinar cells.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- The subcellular localization of type I p21-activated kinases is controlled by the disordered variable region and polybasic sequences.The Journal of biological chemistry · 2019Article
- Mbt/PAK4 together with SRC modulates N-Cadherin adherens junctions in the developingBiology open · 2019Article
- Group I Paks are essential for epithelial- mesenchymal transition in an Apc-driven model of colorectal cancer.Nature communications · 2018Article
- Article
- Rho GTPase effectors and NAD metabolism in cancer immune suppression.Expert opinion on therapeutic targets · 2018Review
- PAR-Complex and Crumbs Function During Photoreceptor Morphogenesis and Retinal Degeneration.Frontiers in cellular neuroscience · 2018Review
- Aberrantly activated Cox-2 and Wnt signaling interact to maintain cancer stem cells in glioblastoma.Oncotarget · 2017Article
- Functional role and therapeutic targeting of p21-activated kinase 4 in multiple myeloma.Blood · 2017Article
- Deciphering the link between PI3K and PAK: An opportunity to target key pathways in pancreatic cancer?Oncotarget · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The serine/threonine kinase PAK4 is a Cdc42 effector whose role is not well understood; overexpression of PAK4 has been associated with some cancers, and there are reports that correlate kinase level with increased cell migration in vitro. Here we report that PAK4 is primarily associated with cell-cell junctions in all the cell lines we tested, and fails to accumulate at focal adhesions or at the leading edge of migrating cells. In U2OS osteosarcoma and MCF-7 breast cancer cell lines, PAK4 depletion did not affect collective cell migration, but affected cell polarization. By contrast, Cdc42 depletion (as reported by many studies) caused a strong defect in junctional assembly in multiple cells lines. We also report that the depletion of PAK4 protein or treatment of cells with the PAK4 inhibitor PF-3758309 can lead to defects in centrosome reorientation (polarization) after cell monolayer wounding. These experiments are consistent with PAK4 forming part of a conserved cell-cell junctional polarity Cdc42 complex. We also confirm β-catenin as a target for PAK4 in these cells. Treatment of cells with PF-3758309 caused inhibition of β-catenin Ser-675 phosphorylation, which is located predominantly at cell-cell junctions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.