Axin localizes to mitotic spindles and centrosomes in mitotic cells

Kim, Sang Hyun; Choi, Eun Jin; Song, Ki Joon; Seo, Eul Ju; Jho, Eek‐hoon; Kee, Sun Ho

doi:10.1016/j.yexcr.2009.01.013

Cited by 35 publications

(47 citation statements)

References 38 publications

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“…HSV-1-mediated cell death requires viral replication and de novo protein synthesis L-EV and L-axin cells were infected with UV-irradiated HSV-1 to determine whether the axin-mediated reduction in cell death was caused by engagement of the virus-receptor A reduction in axin expression by siAxin transfection was confirmed by immunoprecipitation using the E5 mAb and immunoblot analysis using mAb G4, as previously described (Kim et al, 2009). Results are representative of three independent experiments.…”

Section: Resultsmentioning

confidence: 99%

Axin expression enhances herpes simplex virus type 1 replication by inhibiting virus-mediated cell death in L929 cells

Choi

Kim

Jho

et al. 2013

Journal of General Virology

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Herpes simplex virus type 1 (HSV-1) replicates in various cell types and induces early cell death, which limits viral replication in certain cell types. Axin is a scaffolding protein that regulates Wnt signalling and participates in various cellular events, including cellular proliferation and cell death. The effects of axin expression on HSV-1 infection were investigated based on our initial observation that Wnt3a treatment or axin knockdown reduced HSV-1 replication. L929 cells expressed the axin protein in a doxycycline-inducible manner (L-axin) and enhanced HSV-1 replication in comparison to control cells (L-EV). HSV-1 infection induced cell death as early as 6 h after infection through the necrotic pathway and required de novo protein synthesis in L929 cells. Subsequent analysis of viral protein expression suggested that axin expression led to suppression of HSV-1-induced premature cell death, resulting in increased late gene expression. In analysis of axin deletion mutants, the regulators of the G-protein signalling (RGS) domain were involved in the axin-mediated enhancement of viral replication and reduction in cell death. These results suggest that viral replication enhancement might be mediated by the axin RGS domain.

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Section: Resultsmentioning

confidence: 99%

Axin expression enhances herpes simplex virus type 1 replication by inhibiting virus-mediated cell death in L929 cells

Choi

Kim

Jho

et al. 2013

Journal of General Virology

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“…Disruption of PLK1 decreases the stability of Tankryase 1 and leads to a reduction of its PARP activity. Interestingly, phosphorylation of Tankyrase by PLK1 was also shown to affect mitotic spindle assembly (see below) and the regulation of telomeric ends [79]. PLK1 also mediates phosphorylation of Dishevelled2 [152].…”

Section: Tankyrasesmentioning

confidence: 98%

“…Finally, Axin as well as several other components of the degradation complex (GSK3, -catenin, Tankyrase and APC) may colocalize to centrosomes and mitotic spindles [75][76][77][78], where Axin modulates the distribution of Axin associated-proteins such as PLK1 (Serine/threonine-protein kinase, also known as polo-like kinase 1) and GSK3, thereby modulating the mitotic process [79].…”

Section: J01-017amentioning

confidence: 99%

Wnt/beta-Catenin Signaling and Small Molecule Inhibitors

Voronkov¹,

Krauß²

2012

CPD

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Wnt/ -catenin signaling is a branch of a functional network that dates back to the first metazoans and it is involved in a broad range of biological systems including stem cells, embryonic development and adult organs. Deregulation of components involved in Wnt/ -catenin signaling has been implicated in a wide spectrum of diseases including a number of cancers and degenerative diseases. The key mediator of Wnt signaling, -catenin, serves several cellular functions. It functions in a dynamic mode at multiple cellular locations, including the plasma membrane, where -catenin contributes to the stabilization of intercellular adhesive complexes, the cytoplasm where -catenin levels are regulated and the nucleus where -catenin is involved in transcriptional regulation and chromatin interactions. Central effectors of -catenin levels are a family of cysteine-rich secreted glycoproteins, known as Wnt morphogens. Through the LRP5/6-Frizzled receptor complex, Wnts regulate the location and activity of the destruction complex and consequently intracellularcatenin levels. However, -catenin levels and their effects on transcriptional programs are also influenced by multiple other factors including hypoxia, inflammation, hepatocyte growth factor-mediated signaling, and the cell adhesion molecule E-cadherin. The broad implications of Wnt/ -catenin signaling in development, in the adult body and in disease render the pathway a prime target for pharmacological research and development. The intricate regulation of -catenin at its various locations provides alternative points for therapeutic interventions.

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“…13 Axin-1 and Axin-2 also have been localized to centrosomes. Axin-1 might play a role for microtubule nucleation and microtubule stabilization, 14,15 whereas Axin-2 appears to be involved in the regulation of centrosome cohesion. 16 Furthermore, GSK3 has been implicated in the regulation of microtubule dynamics and is required for proper chromosome alignment.…”

Section: Additional Functions Of Wnt Pathway Components During Mitosismentioning

confidence: 99%