Cited by 730Wnt/β-catenin signaling in development and cancerSignaling Pathways in DiseaseProtein Kinase Regulation and GTPase Signaling

Wnt and calcium signaling: β-Catenin-independent pathways

Kohn, Aimee D., Moon, Randall T.·2005·Cell Calcium

Abstract

Wnt signaling is a complex pathway in which beta-catenin is typically viewed as a central mediator. However, within the past 15 years, at least three Wnt-mediated pathways have been proposed that function independent of beta-catenin. One pathway involves activation of calcium/calmodulin-dependent kinase II (CamKII) and protein kinase C (PKC). Another includes recruitment of heterotrimeric GTP-binding proteins to activate phospholipase C (PLC) and phosphodiesterase (PDE). Lastly, a pathway similar to the planar cell polarity (PCP) pathway in Drosophila has been identified that activates the Jun-N-terminal kinase (JNK) and, perhaps, small GTP-binding proteins. Calcium has been implicated as an important second messenger in all of these pathways. This review will focus on the role of calcium in Wnt signaling and, as a consequence, provide a limited overview of beta-catenin-independent Wnt signaling.

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Crossref · 10.1016/j.ceca.2005.06.022

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62 of 62 references verified0 citation errors · 0 not checkable

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  • The Wnt/Ca2+ pathway emerged with the finding that some Wnts and Fz receptors can stimulate intracellular Ca2+ release from ER and this pathway is dependent on G-proteins.

    “The Wnt/Ca2+ pathway emerged with the finding that some Wnts and Fz receptors can stimulate intracellular Ca2+ release from ER and this pathway is dependent on G-proteins.90,91”

    From Wnt signal transduction pathways (2008) · cites this paper as [90]

  • Wnt signaling can proceed through the canonical Wnt/β-catenin pathway or through multiple non-canonical pathways, some of which involve Ca2+ signaling.

    “Signaling downstream of the proteolipid ligands known as Wnts can proceed via the canonical Wnt/β-catenin pathway (Nelson and Nusse, 2004), or through multiple non-canonical pathways, not mediated by β-catenin (Gordon and Nusse, 2006; Rosso et al., 2005; Salinas and Zou, 2008), with some involving Ca2+ signaling (Kohn and Moon, 2005).”

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Authors
Kohn, A. D., & Moon, R. T.
Affiliations
Howard Hughes Medical Institute (US)
Corresponding author
Moon, Randall T.
Venue
Cell Calcium
Publisher
Elsevier BV
Published
2005-09
Volume
38
Issue
3-4
Pages
439-446
ISSN
0143-4160 (ISSN-L)
OpenAlex
W2100701799
Cited by
730
References
61
Citations by year
2026: 13 · 2025: 21 · 2024: 19 · 2023: 27 · 2022: 37 · 2021: 37 · 2020: 23 · 2019: 31 · 2018: 29 · 2017: 46 · 2016: 27 · 2015: 39 · 2014: 48 · 2013: 47 · 2012: 54
FWCI
11.21
Type
journal article
Language
en
Open access
closed
Locations
  • Cell Calcium (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1f32hd049208-01)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (1 F32 HD049208-01)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
Wnt signaling, β-catenin-independent signaling, calcium signaling, calcium/calmodulin-dependent kinase II, protein kinase C, heterotrimeric G proteins, phospholipase C, phosphodiesterase, planar cell polarity pathway, Jun N-terminal kinase, small GTPases, second messengers
MeSH terms
Animals, Humans, Signal Transduction, Calcium Signaling, Wnt Proteins, beta Catenin

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