The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.
Requirement for PAK4 in the Anchorage-independent Growth of Human Cancer Cell Lines
Open accessAbstract
p21-activated protein kinase (PAK) serine/threonine kinases are important effectors of Rho family GTPases and have been implicated in the regulation of cell morphology and motility, as well as in cell transformation. To further investigate the possible involvement of PAK kinases in tumorigenesis, we analyzed the expression of several family members in tumor cell lines. Here we demonstrate that PAK4 is frequently overexpressed in human tumor cell lines of various tissue origins. We also have identified serine (Ser-474) as the likely autophosphorylation site in the kinase domain of PAK4 in vivo. Mutation of this serine to glutamic acid (S474E) results in constitutive activation of the kinase. Phosphospecific antibodies directed against serine 474 detect activated PAK4 on the Golgi membrane when PAK4 is co-expressed with activated Cdc42. Furthermore, expression of the active PAK4 (S474E) mutant has transforming potential, leading to anchorage-independent growth of NIH3T3 cells. A kinase-inactive PAK4 (K350A,K351A), on the other hand, efficiently blocks transformation by activated Ras and inhibits anchorage-independent growth of HCT116 colon cancer cells. Taken together, our data strongly implicate PAK4 in oncogenic transformation and suggest that PAK4 activity is required for Ras-driven, anchorage-independent growth.
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A homologue of Drosophila aurora kinase is oncogenic and amplified in human colorectal cancers
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Self-citationActivation of LIM-kinase by Pak1 couples Rac/Cdc42 GTPase signalling to actin cytoskeletal dynamics
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An essential role for Rac in Ras transformation
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Self-citationPAK Kinases Are Directly Coupled to the PIX Family of Nucleotide Exchange Factors
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Cdc42 and Rac1 induce integrin-mediated cell motility and invasiveness through PI(3)K
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Cited by
Ras superfamily GEFs and GAPs: validated and tractable targets for cancer therapy?
Vigil, D., Cherfils, J., Rossman, K. L., & Der, C. J. (2010) · Nature Reviews Cancer · doi:10.1038/nrc2960 · Cited by 819
p21-Activated kinases: three more join the Pak
Jaffer, Z. M., & Chernoff, J. (2002) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/s1357-2725(01)00158-3 · Cited by 373
PAK4 mediates morphological changes through the regulation of GEF-H1
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Metadata
- Authors
- Callow, M. G., Clairvoyant, F., Zhu, S., Schryver, B., Whyte, D. B., Bischoff, J. R., Jallal, B., & Smeal, T.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2002-01
- Volume
- 277
- Issue
- 1
- Pages
- 550-558
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2025646149
- Cited by
- 288
- References
- 67
- FWCI
- 3.78
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Callow, M. G., Clairvoyant, F., Zhu, S., Schryver, B., Whyte, D. B., Bischoff, J. R., Jallal, B., & Smeal, T. (2002). Requirement for PAK4 in the Anchorage-independent Growth of Human Cancer Cell Lines. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m105732200
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