Hippocampal development and neural stem cell maintenance require Sox2-dependent regulation of Shh
By R. Favaro, Menella Valotta, A. Ferri, E. Latorre, J. Mariani, C. Giachino, Cesare Lancini, V. Tosetti, S. Ottolenghi, V. Taylor and 1 more. 2009
530 citations recorded by the source corpus.
Subfields: Developmental Neuroscience, Molecular Biology
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Developmental Neuroscience
- Fred H. Gage
- Hongjun Song
- Guo-li Ming
- Sebastian Jessberger
- Arturo Alvarez-Buylla
- Gerd Kempermann
- K. Vadodaria
- D. C. Lie
In Molecular Biology
- Hongjun Song
- Guo-li Ming
- Fred H. Gage
- Arturo Alvarez-Buylla
- D. Lagace
- Jagroop Dhaliwal
- Sebastian Jessberger
- D. C. Lie
Citations in the corpus
- Adult Neurogenesis in the Mammalian Brain: Significant Answers and Significant Questions (2011, background): “Shh appears to be a direct target of Sox2 in neural precursors and deletion of Sox2 in adult mice results in a loss of hippocampal neurogenesis (Favaro et al., 2009).”
- Signaling through BMPR-IA regulates quiescence and long-term activity of neural stem cells in the adult hippocampus. (2010, background): “Among the endogenous molecules that are expressed in the dentate gyrus of rodents and that have been shown to regulate hippocampal NSCs, Shh (Favaro et al., 2009) and Wnt3 (Lie et al., 2005) may be relevant (Figure S7).”
- Adult Neurogenesis in the Hippocampus: From Stem Cells to Behavior. (2016, unknown): “Finally, Sox2 was found to modulate Shh signaling by controlling the expression of Shh (Favaro et al., 2009), as well as to inhibit the Wnt signaling-induced transcriptional activation of NeuroD, thereby preventing neuronal differentiation (Kuwabara et al.”
- Quiescent and active hippocampal neural stem cells with distinct morphologies respond selectively to physiological and pathological stimuli and aging. (2010, background): “Although recent evidence indicates that Sox2 is important for hippocampal NSCs, activating sonic hedgehog and regulating Wnt activity, the mechanisms controlling DG NSC maintenance and differentiation are not well understood (Favaro et al., 2009; Kuwabara et al., 2009).”
- The role of adult hippocampal neurogenesis in brain health and disease (2018, background): “Transcription factors Type1 Maintenance of RGLs REST [223, 224], Sox2 [225], Hes5 [216], FoxO [226], NFIX [191], NFIB [227] Activation of RGLs Ascl1 [228, 229]”
- Visualization and genetic manipulation of adult neurogenesis using transgenic mice (2011, background): “transgenic mice that have specific expression in the neurogenic regions in the adult brain have been well characterized in the SGZ with expression in the Sox2 ⁄ GFAP radial glial Type 1 cells (Favaro et al., 2009).”
- RBPJκ-Dependent Signaling Is Essential for Long-Term Maintenance of Neural Stem Cells in the Adult Hippocampus (2010, methodology): “Recent work by Favaro et al. (2009) has demonstrated that the transcription factor Sox2 is essential for adult hippocampal NSC maintenance.”
- Sox1 marks an activated neural stem/progenitor cell in the hippocampus (2012, background): “The Sox transcription factors are central regulators of neurodevelopment (Pevny and Placzek, 2005; Wegner and Stolt, 2005; Favaro et al., 2009; Scott et al., 2010).”
- The germinal matrices in the developing dentate gyrus are composed of neuronal progenitors at distinct differentiation stages (2013, background): “Gene knockout studies indicated that these TFs are important for differentiation of GCs. Sox2 is required for NSC maintenance in the postnatal DG, and deletion of Sox2 leads hypoplasia of the postnatal DG (Favaro et al., 2009).”
- Prospero-related homeobox 1 gene (Prox1) is regulated by canonical Wnt signaling and has a stage-specific role in adult hippocampal neurogenesis (2011, background): “A hypothetical picture emerging is that the nuclear orphan receptor TLX (33) and Sry-related HMG box transcription factors such as SOX2 and SOX9 maintain hippocampal NSCs in an undifferentiated state (24, 33, 34).”