RanBP3 enhances nuclear export of active β-catenin independently of CRM1

Hendriksen, Jolita; Fagotto, François; Velde, Hella van der; Schie, Martijn van; Noordermeer, Jasprina N.; Fornerod, Maarten

doi:10.1083/jcb.200502141

Cited by 80 publications

(85 citation statements)

References 79 publications

(91 reference statements)

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“…For nuclear export of β-catenin there is evidence that β-catenin may exit via binding to proteins such as Axin (12) and APC (10) using a Ran and CRM1-independent mechanism (11). Alternatively, β-catenin can interact with RanBP3 to be exported from the nucleus (14). In the present work we show that Custos inhibits canonical Wnt signaling in frog embryos and cultured cells by antagonizing nuclear import of β−catenin.…”

supporting

confidence: 48%

Custos controls β-catenin to regulate head development during vertebrate embryogenesis

Komiya

Mandrekar

Sato

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Precise control of the canonical Wnt pathway is crucial in embryogenesis and all stages of life, and dysregulation of this pathway is implicated in many human diseases including cancers and birth defect disorders. A key aspect of canonical Wnt signaling is the cytoplasmic to nuclear translocation of β-catenin, a process that remains incompletely understood. Here we report the identification of a previously undescribed component of the canonical Wnt signaling pathway termed Custos, originally isolated as a Dishevelledinteracting protein. Custos contains casein kinase phosphorylation sites and nuclear localization sequences. In Xenopus, custos mRNA is expressed maternally and then widely throughout embryogenesis. Depletion or overexpression of Custos produced defective anterior head structures by inhibiting the formation of the Spemann-Mangold organizer. In addition, Custos expression blocked secondary axis induction by positive signaling components of the canonical Wnt pathway and inhibited β-catenin/TCF-dependent transcription. Custos binds to β-catenin in a Wnt responsive manner without affecting its stability, but rather modulates the cytoplasmic to nuclear translocation of β-catenin. This effect on nuclear import appears to be the mechanism by which Custos inhibits canonical Wnt signaling. The function of Custos is conserved as loss-of-function and gainof-function studies in zebrafish also demonstrate a role for Custos in anterior head development. Our studies suggest a role for Custos in fine-tuning canonical Wnt signal transduction during embryogenesis, adding an additional layer of regulatory control in the Wnt-β-catenin signal transduction cascade.

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supporting

confidence: 48%

Custos controls β-catenin to regulate head development during vertebrate embryogenesis

Komiya

Mandrekar

Sato

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…Knockdown of WEE1 promotes G2/M progression and sensitizes stathmin-overexpressing breast cancer cells to paclitaxel and vinblastine [48]. RANBP3 ablation causes overactivation of Wnt signaling pathway, and the chromosome region 19p13.3 containing the RANBP3 gene is deleted in various types of cancers and may contain tumor suppressor gene [49]. Three promising genes (LTBR, EI24 and SMAD2) were identified as targets of miR-455-3p.…”

Section: Discussionmentioning

confidence: 99%

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

Ujifuku¹,

Mitsutake²,

Takakura³

et al. 2010

Cancer Letters

209

137

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Running title: miRNAs and temozolomide resistance in glioblastoma Key words: glioblastoma, resistance, microRNA,, miR-10a*, temozolomide. ABSTRACTTo identify microRNAs (miRNAs) specifically involved in the acquisition of temozolomide (TMZ) resistance in glioblastoma multiforme (GBM), we first established a resistant variant, U251R cells from TMZ-sensitive GBM cell line, U251MG. We then performed a comprehensive analysis of miRNA expressions in U251R and parental cells using miRNA microarrays. miR-195, miR-455-3p and miR-10a* were the three most up-regulated miRNAs in the resistant cells. To investigate the functional role of these miRNAs in TMZ resistance, U251R cells were transfected with miRNA inhibitors consisting of DNA/LNA hybrid oligonucleotides. Suppression of miR-455-3p or miR-10a* had no effect on cell growth, but showed modest cell killing effect in the presence of TMZ. On the other hand, knockdown of miR-195 alone displayed moderate cell killing effect, and combination with TMZ strongly enhanced the effect. In addition, using in silico analysis combined with cDNA microarray experiment, we present possible mRNA targets of these miRNAs. In conclusion, our findings suggest that those miRNAs may play a role in acquired TMZ resistance and could be a novel target for recurrent GBM treatment.

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“…115,116 Furthermore, RanBP3 has been shown to be involved in nuclear export of ␤-catenin. 117 In the nucleus, Bcl9 and pygopus play a role in retention of ␤-catenin. 118 In detailed fluorescence recovery after photobleaching experiments, it was recently shown that APC, axin, Bcl9, and TCF factors influence the cytoplasmic/nuclear localization of ␤-catenin mainly on the level of retention rather than active transport.…”

Section: Regulating Nuclear Localization Of ␤-Cateninmentioning

confidence: 99%

An Updated Overview on Wnt Signaling Pathways

Tata

Kühl

2010

Circulation Research

596

502

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Growth factor signaling is required for cellular differentiation, tissue morphogenesis, and tissue homeostasis.Misregulation of intracellular signal transduction can lead to developmental defects during embryogenesis or particular diseases in the adult. One family of growth factors important for these aspects is given by the Wnt proteins. In particular, Wnts have important functions in stem cell biology, cardiac development and differentiation, angiogenesis, cardiac hypertrophy, cardiac failure, and aging. Knowledge of growth factor signaling during differentiation will allow for improvement of targeted differentiation of embryonic or adult stem cells toward functional cardiomyocytes or for understanding the basis of diseases. Our major aim here is to provide a state of the art review summarizing our present knowledge of the intracellular Wnt-mediated signaling network. In particular, we provide evidence that the subdivision into canonical and noncanonical Wnt signaling pathways solely based on the identity of Wnt ligands or Frizzled receptors is not appropriate anymore. We thereby deliver a solid base for further upcoming articles of a review series focusing on the role of Wnt proteins on different aspects of cardiovascular development and dysfunction.

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RanBP3 enhances nuclear export of active β-catenin independently of CRM1

Cited by 80 publications

References 79 publications

Custos controls β-catenin to regulate head development during vertebrate embryogenesis

Custos controls β-catenin to regulate head development during vertebrate embryogenesis

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

An Updated Overview on Wnt Signaling Pathways

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