PMID- 10395542
OWN - NLM
STAT- MEDLINE
DCOM- 19990917
LR  - 20190613
IS  - 0960-9822 (Print)
IS  - 0960-9822 (Linking)
VI  - 9
IP  - 13
DP  - 1999 Jul 1
TI  - Protein kinase C is differentially stimulated by Wnt and Frizzled homologs in a
      G-protein-dependent manner.
PG  - 695-8
AB  - In studies of developmental signaling pathways stimulated by the Wnt proteins and
      their receptors, Xenopus Wnt-5A (Xwnt-5A) and a prospective Wnt receptor, rat
      Frizzled 2 (Rfz2), have been shown to stimulate inositol signaling and Ca2+
      fluxes in zebrafish [1] [2] [3]. As protein kinase C (PKC) isoforms can respond
      to Ca2+ signals [4], we asked whether expression of different Wnt and Frizzled
      homologs modulates PKC. Expression of Rfz2 and Xwnt-5A resulted in translocation 
      of PKC to the plasma membrane, whereas expression of rat Frizzled 1 (Rfz1), which
      activates a Wnt pathway using beta-catenin but not Ca2+ fluxes [5], did not. Rfz2
      and Xwnt-5A were also able to stimulate PKC activity in an in vitro kinase assay.
      Agents that inhibit Rfz2-induced signaling through G-protein subunits blocked
      Rfz2-induced translocation of PKC. To determine if other Frizzled homologs
      differentially stimulate PKC, we tested mouse Frizzled (Mfz) homologs for their
      ability to induce PKC translocation relative to their ability to induce the
      expression of two target genes of beta-catenin, siamois and Xnr3. Mfz7 and Mfz8
      stimulated siamois and Xnr3 expression but not PKC activation, whereas Mfz3, Mfz4
      and Mfz6 reciprocally stimulated PKC activation but not expression of siamois or 
      Xnr3. These results demonstrate that some but not all Wnt and Frizzled signals
      modulate PKC localization and stimulate PKC activity via a G-protein-dependent
      mechanism. In agreement with other studies [1] [2] [3]. [6] [7] these data
      support the existence of multiple Wnt and Frizzled signaling pathways in
      vertebrates.
FAU - Sheldahl, L C
AU  - Sheldahl LC
AD  - Howard Hughes Medical Institute, Department of Pharmacology, Center for
      Developmental Biology, University of Washington School of Medicine, Seattle,
      Washington, 98195, USA.
FAU - Park, M
AU  - Park M
FAU - Malbon, C C
AU  - Malbon CC
FAU - Moon, R T
AU  - Moon RT
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Curr Biol
JT  - Current biology : CB
JID - 9107782
RN  - 0 (CTNNB1 protein, Xenopus)
RN  - 0 (CTNNB1 protein, mouse)
RN  - 0 (Ctnnb1 protein, rat)
RN  - 0 (Cytoskeletal Proteins)
RN  - 0 (Eye Proteins)
RN  - 0 (Glycoproteins)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (Proteins)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (SIA1 protein, Xenopus)
RN  - 0 (Sfrp2 protein, mouse)
RN  - 0 (Trans-Activators)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (WD repeat containing planar cell polarity effector)
RN  - 0 (Wnt Proteins)
RN  - 0 (Wnt-5a Protein)
RN  - 0 (Wnt5a protein, Xenopus)
RN  - 0 (Xenopus Proteins)
RN  - 0 (beta Catenin)
RN  - 0 (nodal3.1 protein, Xenopus)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cytoskeletal Proteins/metabolism
MH  - Eye Proteins/metabolism
MH  - GTP-Binding Proteins/metabolism
MH  - Glycoproteins/metabolism
MH  - Homeodomain Proteins/metabolism
MH  - Intracellular Signaling Peptides and Proteins
MH  - *Membrane Proteins
MH  - Mice
MH  - Microscopy, Confocal
MH  - Polymerase Chain Reaction
MH  - Protein Kinase C/*metabolism
MH  - Proteins/metabolism
MH  - Rats
MH  - Receptors, Transforming Growth Factor beta/metabolism
MH  - *Trans-Activators
MH  - *Transforming Growth Factor beta
MH  - Wnt Proteins
MH  - Wnt-5a Protein
MH  - Xenopus
MH  - *Xenopus Proteins
MH  - beta Catenin
EDAT- 1999/07/08 00:00
MHDA- 1999/07/08 00:01
CRDT- 1999/07/08 00:00
PHST- 1999/07/08 00:00 [pubmed]
PHST- 1999/07/08 00:01 [medline]
PHST- 1999/07/08 00:00 [entrez]
AID - S0960-9822(99)80310-8 [pii]
PST - ppublish
SO  - Curr Biol. 1999 Jul 1;9(13):695-8.