45
Views
108
CrossRef citations to date
0
Altmetric
Cell Growth and Development

Cell-Type-Specific Activation of PAK2 by Transforming Growth Factor β Independent of Smad2 and Smad3

, , &
Pages 8878-8889 | Received 08 May 2003, Accepted 21 Aug 2003, Published online: 27 Mar 2023

REFERENCES

  • Anders, R. A., J. E. J. Doré, S. A. Arline, N. Garamszegi, and E. B. Leof. 1998. Differential requirements for type I and type II TGFβ receptor kinase activity in ligand-mediated receptor endocytosis. J. Biol. Chem. 273: 23118–23125.
  • Anders, R. A., and E. B. Leof. 1996. Chimeric granulocyte/macrophage colony-stimulating factor/transforming growth factor-β (TGF-β) receptors define a model system for investigating the role of homomeric and heteromeric receptors in TGF-β signaling. J. Biol. Chem. 271: 21758–21766.
  • Bagrodia, S., and R. A. Cerione. 1999. PAK to the future. Trends Cell Biol. 9: 350–355.
  • Bhowmick, N. A., M. Ghiassi, A. Bakin, M. Aakre, C. A. Lundquist, M. E. Engel, C. L. Arteaga, and H. L. Moses. 2001. Transforming growth factor-β1 mediates epithelial to mesenchymal transdifferentiation through a RhoA-dependent mechanism. Mol. Biol. Cell 12: 27–36.
  • Bissell, D. M. 2001. Chronic liver injury, TGF-β, and cancer. Exp. Mol. Med. 33: 179–190.
  • Blobe, G. C., W. P. Schiemann, and H. F. Lodish. 2000. Role of transforming growth factor beta in human disease. N. Engl. J. Med. 342: 1350–1358.
  • Bokoch, G. M. 2000. Regulation of cell function by Rho family GTPase. Immunol. Res. 21: 139–148.
  • Bono, F., I. Lamarche, and J. Herbert. 1997. NGF exhibits a pro-apoptotic activity for human vascular smooth muscle cells that is inhibited by TGF-β1. FEBS Lett. 416: 243–246.
  • Callow, M. G., F. Clairvoyant, S. Zhu, B. Schryver, D. B. Whyte, J. R. Bischoff, B. Hallal, and T. Smeal. 2002. Requirement for PAK4 in the anchorage-independent growth of human cancer cell lines. J. Biol. Chem. 277: 550–558.
  • Chambard, J.-C., and J. Pouyssegur. 1988. TGF-β inhibits growth factor-induced DNA synthesis in hamster fibroblasts without affecting early mitogenic events. J. Cell. Physiol. 135: 101–107.
  • Chen, R., Y. Su, R. L. C. Chuang, and T. Chang. 1998. Suppression of transforming growth factor-β-induced apoptosis through phosphatidylinositol 3-kinase/akt-dependent pathway. Oncogene 17: 1959–1968.
  • Chen, Y., and T. Tan. 1999. Mammalian c-Jun N-terminal kinase pathway and STE20-related kinases. Gene Ther. Mol. Biol. 4: 83–98.
  • Cogan, J. G., S. V. Subramanian, J. A. Polikandriotis, R. J. Kelm, and A. R. Strauch. 2002. Vascular smooth muscle α-actin gene transcription during myofibroblast differentiation requires Sp1/3 protein binding proximal to the MCAT enhancer. J. Biol. Chem. 277: 36433–36442.
  • Doré, J. J. E., Jr., M. Edens, N. Garamszegi, and E. B. Leof. 1998. Heteromeric and homomeric transforming growth factor-β receptors show distinct signaling and endocytic responses in epithelial cells. J. Biol. Chem. 273: 31770–31777.
  • Edwards, D. C., L. C. Sanders, G. M. Bokoch, and G. N. Gill. 1999. Activation of LIM-kinase by PAK1 couples Rac/Cdc42 GTPase signaling to actin cytoskeletal dynamics. Nat. Cell Biol. 1: 253–259.
  • Engel, M. E., M. A. McDonnell, B. K. Law, and H. L. Moses. 1999. Interdependent SMAD and JNK signaling in TGF-β mediated transcription. J. Biol. Chem. 274: 37413–37420.
  • Flanders, K. C., C. D. Sullivan, M. Fujii, A. Sowers, M. A. Anzano, A. Arabshahi, C. Major, C. Deng, A. Russo, J. B. Mitchell, and A. B. Roberts. 2002. Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation. Am. J. Pathol. 160: 1057–1068.
  • Garamszegi, N., J. J. E. Doré, Jr., S. G. Penheiter, M. Edens, D. Yao, and E. B. Leof. 2001. Transforming growth factor β receptor signaling and endocytosis are linked through a COOH terminal activation motif in the type I receptor. Mol. Biol. Cell 12: 2881–2893.
  • Hashimoto, S., Y. Gon, I. Takeshita, K. Matsumoto, S. Maruoka, and T. Horie. 2001. Transforming growth factor-β1 induces phenotypic modulation of human lung fibroblasts to myofibroblasts through a c-Jun-NH2-terminal kinase-dependent pathway. Am. J. Respir. Crit. Care Med. 163: 152–157.
  • Hayes, S., A. Chawla, and S. Corvera. 2002. TGFβ receptor internalization into EEA1-enriched early endosomes: role in signaling to Smad2. J. Cell Biol. 158: 1239–1249.
  • He, H., A. Levitzki, H.-J. Zhu, F. Walker, A. Burgess, and H. Maruta. 2001. Platelet-derived growth factor requires epidermal growth factor receptor to activate p21-activated kinase family kinases. J. Biol. Chem. 276: 26741–26744.
  • Hocevar, B. A., T. L. Brown, and P. H. Howe. 1999. TGF-β induces fibronectin synthesis through a c-Jun N-terminal kinase-dependent, Smad4-independent pathway. EMBO J. 18: 1345–1356.
  • Hocevar, B. A., A. Smine, X.-X. Xu, and P. H. Howe. 2001. The adaptor molecule disabled-2 links the transforming growth factor β receptors to the Smad pathway. EMBO J. 20: 2789–2801.
  • Howe, P. H., G. Draetta, and E. B. Leof. 1991. Transforming growth factor β1 inhibition of p34cdc2 phosphorylation and histone H1 kinase activity is associated with G1/S-phase growth arrest. Mol. Cell. Biol. 11: 1185–1194.
  • Jaffer, Z. M., and J. Chernoff. 2002. p21-activated kinases: three more join the Pak. Int. J. Biochem. Cell Biol. 34: 713–717.
  • Knaus, U. G., and G. M. Bokoch. 1998. The p21Rac-Cdc42-activated kinases (PAKs). Int. J. Biochem. Cell Biol. 30: 857–862.
  • Lei, M., W. Lu, W. Meng, M. Parrini, M. J. Eck, B. J. Mayer, and S. C. Harrison. 2000. Structure of PAK1 in an autoinhibited conformation reveals a multistage activation switch. Cell 102: 387–397.
  • Manser, E., T.-H. Loo, C.-G. Koh, Z.-S. Zhao, X.-Q. Chen, L. Tan, I. Tan, T. Leung, and L. Lim. 1998. PAK kinases are directly coupled to the PIX family of nucleotide exchange factors. Mol. Cell 1: 183–192.
  • Massagué, J., and Y.-G. Chen. 2000. Controlling TGF-β signaling. Genes Dev. 14: 627–644.
  • Massagué, J., and D. Wotton. 2000. Transcriptional control by the TGF-β/Smad signaling system. EMBO J. 1745–1754.
  • Penheiter, S. G., H. Mitchell, N. Garamszegi, M. Edens, J. J. E. Doré, Jr., and E. B. Leof. 2002. Internalization-dependent and -independent requirements for transforming growth factor β receptor signaling via the Smad pathway. Mol. Cell. Biol. 22: 4750–4759.
  • Piek, E., W. J. Ju, J. Heyer, D. Escalante-Alcalde, C. L. Stewart, M. Weinstein, C. Deng, R. Kucherlapati, E. P. Büttinger, and A. B. Roberts. 2001. Functional characterization of transforming growth factor β signaling in Smad2- and Smad3-deficient fibroblasts. J. Biol. Chem. 276: 19945–19953.
  • Prunier, C., A. Mazars, V. Noë, E. Bruyneel, M. Mareel, C. Gespach, and A. Afti. 1999. Evidence that Smad2 is a tumor suppressor implicated in the control of cellular invasion. J. Biol. Chem. 274: 22919–22922.
  • Qu, J., M. S. Cammarano, Q. Shi, K. C. Ha, P. de Lanerolle, and A. Minden. 2001. Activated PAK4 regulates cell adhesion and anchorage-independent growth. Mol. Cell. Biol. 21: 3523–3533.
  • Raftery, L. A., V. Twombly, K. Wharton, and W. M. Gelbart. 1995. Genetic screens to identify elements of the decapentaplegic signaling pathway in drosophila. Genetics 139: 241–254.
  • Roig, J., Z. Huang, C. Lytle, and J. A. Traugh. 2000. p21-activated protein kinase γ-PAK is translocated and activated in response to hyperosmolarity. J. Biol. Chem. 275: 16933–16940.
  • Roig, J., and J. A. Traugh. 2001. Cytostatic p21 G protein-activated protein kinase γ-PAK. Vitam. Horm. 62: 167–198.
  • Roig, J., P. T. Tuazon, P. A. Zipfel, A. M. Pendergast, and J. A. Traugh. 2000. Functional interaction between c-Abl and the p21-activated protein kinase γ-pak. Proc. Natl. Acad. Sci. USA 97: 14346–14351.
  • Royal, I., N. Lamarche, L. Lamorte, K. Kozo, and M. Park. 2000. Activation of Cdc42, Rac, PAK, and Rho-kinase in response to hepatocyte growth factor differentially regulates epithelial cell colony spreading and dissociation. Mol. Biol. Cell 11: 1709–1725.
  • Rudel, T., and G. M. Bokoch. 1997. Membrane and morphological changes in apoptotic cells regulated by caspase-mediated activation of PAK2. Science 276: 1571–1574.
  • Savage, C., P. Das, A. L. Finelli, S. R. Townsend, C.-Y. Sun, S. E. Baird, and R. W. Padgett. 1996. Caenorhabditis elegans genes sma-2, sma-3, and sma-4 define a conserved family of transforming growth factor beta pathway components. Proc. Natl. Acad. Sci. USA 93: 790–794.
  • Schurmann, A., A. F. Mooney, L. C. Sanders, M. A. Sells, H. G. Wang, J. C. Reed, and G. M. Bokoch. 2000. p21-activated kinase 1 phosphorylates the death agonist Bad and protects cells from apoptosis. Mol. Cell. Biol. 20: 453–461.
  • Serini, G., and G. Gabbiani. 1999. Mechanisms of myofibroblast activity and phenotype modulation. Exp. Cell Res. 250: 273–283.
  • Shipley, G. D., C. B. Childs, M. E. Volkenant, and H. L. Moses. 1984. Differential effects of epidermal growth factor, transforming growth factor, and insulin on DNA and protein synthesis and morphology in serum-free cultures of AKR-2B cells. Cancer Res. 44: 710–716.
  • ten Dijke, P., M.-J. Goumans, H. Itoh, and S. Itoh. 2002. Regulation of cell proliferation by Smad proteins. J. Cell. Physiol. 191: 1–16.
  • Wells, C. M., A. Abo, and A. J. Ridley. 2002. PAK4 is activated via P13K in HGF-stimulated epithelial cells. J. Cell Sci. 115: 3947–3956.
  • Yang, F., X. Li, M. Sharma, M. Zarnegar, B. Lim, and Z. Sun. 2001. Androgen receptor specifically interacts with a novel p21-activated kinase, PAK6. J. Biol. Chem. 276: 15345–15353.
  • Yue, J., and K. M. Mulder. 2001. Transforming growth factor-β signal transduction in epithelial cells. Pharmacol. Ther. 91: 1–34.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.