The cell-polarity protein Par6 links Par3 and atypical protein kinase C to Cdc42

By G. Joberty, C. Petersen, Lin Gao, I. Macara. Nature Cell Biology, 2000

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Subfields: Aging, Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/43f436d0fd410de2f33c8e1934c0f32095b61c70

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Citations in the corpus

Tight junctions and cell polarity. (2006, background): “F or p er so na l u se o nl y. Baz: Bazooka with the active form of Cdc42, a Rho GTPase, via its semi-Cdc42/Rac interacting binding (CRIB) domain, and with part of the PDZ domain ( Joberty et al. 2000, Johansson et al. 2000, Lin et al. 2000, Qiu et al. 2000).”
The role of the Rho GTPases in neuronal development. (2005, background): “This protein complex has been shown to interact with activated forms of Rac1 and Cdc42 through mPar6 (Joberty et al. 2000; Johansson et al. 2000) and is required for the generation of anterior–posterior polarity in early C. elegans embryos, the apical–basal polarity of epithelial cells and…”
Renal defects associated with improper polarization of the CRB and DLG polarity complexes in MALS-3 knockout mice (2007, positive): “The second complex includes the PDZ protein PAR-3, which binds to atypical protein kinase C (aPKC) (Izumi et al., 1998), and the PDZ protein PAR-6 (Joberty et al., 2000; Lin et al., 2000).”
Salmonella interactions with host cells: type III secretion at work. (2001, background): “Indeed, Salmonella causes the disruption of tight junctions of the intestinal epithelium (Jepson et al. 1995, 2000), most likely as a consequence of the activation of Rho GTPases by the SPI-1 TTSS (Gopalakrishnan et al. 1998, Joberty et al. 2000).”
PTEN-mediated apical segregation of phosphoinositides controls epithelial morphogenesis through Cdc42. (2007, background): “The Rho-GTPase effector protein Par6 links Par3 and aPKC to activated Cdc42, forming a multimeric polarityregulatory complex at the PM of MDCK cells (Joberty et al., 2000).”
Cell junction dynamics in the testis: Sertoli-germ cell interactions and male contraceptive development. (2002, background): “When either Par6, Par3, or Cdc42 is overexpressed in epithelial cells, it causes dislocation of ZO-1 from the site of TJs, rendering the loss of cell polarity, indicating the Cdc42/Par6/Par3/PKC complex, along with ZO-1, may be critical to maintain cell-cell contact and cell polarity at the site of ”
Tight junctions at the blood brain barrier: physiological architecture and disease-associated dysregulation (2012, positive): “The participation of this PCP complex to TJ integrity was further illustrated by the recent observation that meningococcal adhesion to human cerebral endothelial cells recruited Par-3, Par-6 and aPKC-ζ under bacterial colonies and induced disruption of cell-cell junctions [156].”
Cytokine regulation of tight junctions (2008, background): “Cdc42, a small Rho family GTPase, is thought to act together with Par6 as a GTP dependent molecular switch for the activation of aPKC [77].”