The cell-polarity protein Par6 links Par3 and atypical protein kinase C to Cdc42
- PMID: 10934474
- DOI: 10.1038/35019573
The cell-polarity protein Par6 links Par3 and atypical protein kinase C to Cdc42
Abstract
PAR (partitioning-defective) proteins, which were first identified in the nematode Caenorhabditis elegans, are essential for asymmetric cell division and polarized growth, whereas Cdc42 mediates establishment of cell polarity. Here we describe an unexpected link between these two systems. We have identified a family of mammalian Par6 proteins that are similar to the C. elegans PDZ-domain protein PAR-6. Par6 forms a complex with Cdc42-GTP, with a human homologue of the multi-PDZ protein PAR-3 and with the regulatory domains of atypical protein kinase C (PKC) proteins. This assembly is implicated in the formation of normal tight junctions at epithelial cell-cell contacts. Thus, Par6 is a key adaptor that links Cdc42 and atypical PKCs to Par3.
Comment in
-
Cell polarity: new PARtners for Cdc42 and Rac.Nat Cell Biol. 2000 Aug;2(8):E143-5. doi: 10.1038/35019620. Nat Cell Biol. 2000. PMID: 10934484
Similar articles
-
Cell polarity: new PARtners for Cdc42 and Rac.Nat Cell Biol. 2000 Aug;2(8):E143-5. doi: 10.1038/35019620. Nat Cell Biol. 2000. PMID: 10934484
-
Assembly of epithelial tight junctions is negatively regulated by Par6.Curr Biol. 2002 Feb 5;12(3):221-5. doi: 10.1016/s0960-9822(01)00663-7. Curr Biol. 2002. PMID: 11839275
-
Atypical protein kinase C is involved in the evolutionarily conserved par protein complex and plays a critical role in establishing epithelia-specific junctional structures.J Cell Biol. 2001 Mar 19;152(6):1183-96. doi: 10.1083/jcb.152.6.1183. J Cell Biol. 2001. PMID: 11257119 Free PMC article.
-
Epithelial junctions and Rho family GTPases: the zonular signalosome.Small GTPases. 2014;5(4):1-15. doi: 10.4161/21541248.2014.973760. Small GTPases. 2014. PMID: 25483301 Free PMC article. Review.
-
PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.Cell Mol Life Sci. 2018 Aug;75(15):2735-2761. doi: 10.1007/s00018-018-2828-6. Epub 2018 Apr 25. Cell Mol Life Sci. 2018. PMID: 29696344 Free PMC article. Review.
Cited by
-
Atypical Protein Kinase C Promotes its own Asymmetric Localisation by Phosphorylating Cdc42 in the C. elegans zygote.bioRxiv [Preprint]. 2024 Jun 14:2023.10.27.563985. doi: 10.1101/2023.10.27.563985. bioRxiv. 2024. PMID: 38009101 Free PMC article. Preprint.
-
Cdc42 deficiency causes ciliary abnormalities and cystic kidneys.J Am Soc Nephrol. 2013 Sep;24(9):1435-50. doi: 10.1681/ASN.2012121236. Epub 2013 Jun 13. J Am Soc Nephrol. 2013. PMID: 23766535 Free PMC article.
-
Phosphorylation of E-cadherin at threonine 790 by protein kinase Cδ reduces β-catenin binding and suppresses the function of E-cadherin.Oncotarget. 2016 Jun 14;7(24):37260-37276. doi: 10.18632/oncotarget.9403. Oncotarget. 2016. PMID: 27203386 Free PMC article.
-
Normal establishment of epithelial tight junctions in mice and cultured cells lacking expression of ZO-3, a tight-junction MAGUK protein.Mol Cell Biol. 2006 Dec;26(23):9003-15. doi: 10.1128/MCB.01811-05. Epub 2006 Sep 25. Mol Cell Biol. 2006. PMID: 17000770 Free PMC article.
-
E-cadherin is essential for in vivo epidermal barrier function by regulating tight junctions.EMBO J. 2005 Mar 23;24(6):1146-56. doi: 10.1038/sj.emboj.7600605. Epub 2005 Mar 3. EMBO J. 2005. PMID: 15775979 Free PMC article.
Publication types
MeSH terms
Substances
Associated data
- Actions
- Actions
- Actions
- Actions
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases
Research Materials
Miscellaneous