ArticleDevelopmental biology2017
Spop regulates Gli3 activity and Shh signaling in dorsoventral patterning of the mouse spinal cord.
Article in Developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Large-scale quaternary structural transitions underlie gain of function of SPOP cancer mutations.Molecular cell · 2026Article
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- [Molecular cancer · 2026Article
- Integrated Single-cell Analysis Uncovers Regulatory Logic of Cranial Ectoderm Development.bioRxiv : the preprint server for biology · 2025Article
- The equilibrium between two quaternary assembly states determines the activity of SPOP and its cancer mutants.bioRxiv : the preprint server for biology · 2025Article
- Regulatory mechanisms governing GLI proteins in hedgehog signaling.Anatomical science international · 2025Review
- Cul3 substrate adaptor SPOP targets Nup153 for degradation.Molecular biology of the cell · 2025Article
- Challenges and opportunities for the diverse substrates of SPOP E3 ubiquitin ligase in cancer.Theranostics · 2025Review
- HIB/SPOP inhibits Ci/Gli-mediated tumorigenesis by modulating the RNA Polymerase II components stabilities.iScience · 2023Article
- SPOPL induces tumorigenicity and stemness in glioma stem cells by activating Notch signaling.Journal of neuro-oncology · 2023Article
- TMEM132A regulates mouse hindgut morphogenesis and caudal development.Development (Cambridge, England) · 2023Article
- Nabais Sa-de Vries syndrome in a Chinese infant associated with a novel SPOP mutation: A clinical study and genetic report.Molecular genetics & genomic medicine · 2022Article
- Review
- TMEM132A ensures mouse caudal neural tube closure and regulates integrin-based mesodermal migration.Development (Cambridge, England) · 2022Article
- Regulation of Hedgehog Signal Transduction by Ubiquitination and Deubiquitination.International journal of molecular sciences · 2021Review
- SPOP and CUL3 Modulate the Sonic Hedgehog Signal Response Through Controlled Degradation of GLI Family Transcription Factors.Frontiers in cell and developmental biology · 2021Review
- SPOP and cancer: a systematic review.American journal of cancer research · 2020Review
- SPOP attenuates migration and invasion of choriocarcinoma cells by promoting DHX9 degradation.American journal of cancer research · 2020Article
- Sufu- and Spop-mediated downregulation of Hedgehog signaling promotes beta cell differentiation through organ-specific niche signals.Nature communications · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Sonic Hedgehog (Shh) signaling regulates the patterning of ventral spinal cord through the effector Gli family of transcription factors. Previous in vitro studies showed that an E3 ubiquitin ligase containing Speckle-type POZ protein (Spop) targets Gli2 and Gli3 for ubiquitination and degradation, but the role of Spop in Shh signaling and mammalian spinal cord patterning remains unknown. Here, we show that loss of Spop does not alter spinal cord patterning, but it suppresses the loss of floor plate and V3 interneuron phenotype of Gli2 mutants, suggesting a negative role of Spop in Gli3 activator activity, Shh signaling and the specification of ventral cell fates in the spinal cord. This correlates with a moderate but significant increase in the level of Gli3 protein in the Spop mutant spinal cords. Furthermore, loss of Spop restores the maximal Shh pathway activation and ventral cell fate specification in the Gli1;Sufu double mutant spinal cord. Finally, we show that loss of Spop-like does not change the spinal cord patterning in either wild type or Spop mutants, suggesting that it does not compensate for the loss of Spop in Shh signaling and spinal cord patterning. Therefore, our results demonstrate a negative role of Spop in the level and activity of Gli3, Shh signaling and ventral spinal cord patterning.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.