Hes genes regulate size, shape and histogenesis of the nervous system by control of the timing of neural stem cell differentiation
By J. Hatakeyama, Yasumasa Bessho, K. Katoh, S. Ookawara, M. Fujioka, F. Guillemot, Ryoichiro Kageyama. Development, 2004
622 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/8c09cef00645287e41be6424788e110efaedc889
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- W. Huttner
- A. Kriegstein
- M. Götz
- Jan H. Lui
- David V. Hansen
- Ryoichiro Kageyama
- Masahiro Yamaguchi
- Se Hoon Choi
In Developmental Neuroscience
- W. Huttner
- A. Kriegstein
- M. Götz
- Jan H. Lui
- David V. Hansen
- Ryoichiro Kageyama
- T. Ohtsuka
- Hiromi Shimojo
In Molecular Biology
- A. Kriegstein
- W. Huttner
- M. Götz
- Ryoichiro Kageyama
- T. Ohtsuka
- David V. Hansen
- Jan H. Lui
- Hiromi Shimojo
Citations in the corpus
- Essential Roles of Notch Signaling in Maintenance of Neural Stem Cells in Developing and Adult Brains (2010, background): “We previously generated mouse mutants that lacked the Notch effector genes Hes1, Hes3, and Hes5, and found that virtually all neural stem cells prematurely differentiated into neurons and were depleted in most regions of the CNS (Hatakeyama et al., 2004).”
- Notch signaling in the mammalian central nervous system: insights from mouse mutants (2005, positive): “First, recent work has shown that Hes1 −/− Hes3 −/− Hes5 −/− triple mutants show even more precocious neuronal differentiation than Hes1 −/− Hes5 −/− double mutant”
- Presenilin 1 mutants impair the self-renewal and differentiation of adult murine SVZ-neuronal progenitors via cell autonomous mechanisms involving Notch signaling (2010, methodology): “Extending these observations, we used q-PCR assays to compare the transcript levels of Hes1, Hes5, Hes7, Hey1 and Hey2, the well established candidate target genes of the mammalian Notch pathway (Hatakeyama et al., 2004; Yu et al., 2008) in NPCs derived from the SVZ of adult PS1hWT or PS1 E9 mice (s”
- Development and Evolution of the Human Neocortex (2011, positive): “Cells with higher expression levels stimulate Notch more potently in neighboring cells to induce downstream effectors such as HES1 and HES5, which repress the expression of Delta by transcriptional feedback, thereby diminishing the neighboring cell’s ability to stimulate Notch in the initiating cell”
- The Hes gene family: repressors and oscillators that orchestrate embryogenesis (2007, background): “, 1998) Hes3 CNS, PNS Repression of neurogenesis (Notch-independent) (Hirata et al., 2001; Hatakeyama et al., 2004) Hes4 Exists in human but not in mouse Hes5 CNS, PNS Repression of neurogenesis (Notch-dependent) (Ohtsuka et al.”
- Developmental cell biology: The cell biology of neurogenesis (2005, background): “It will be important to elucidate how such spatial and temporal control mechanisms are coordinated as potential molecular links — for example, HES1 and HES5 (Ref”
- [P2.15]: Oscillations in notch signaling regulate maintenance of neural progenitors (2008, positive): “…Ngn2 and Dll1 not only were repressed by overexpression of Hes1 (Figures 4I and 4K) but also are known to be upregulated in the absence of Hes1 (Hatakeyama et al., 2004; Baek et al., 2006), raising the possibility that expression of Ngn2 and Dll1 dynamically changes under the control of Hes1…”