ArticleGenes & development1997
Mediation of NGF signaling by post-translational inhibition of HES-1, a basic helix-loop-helix repressor of neuronal differentiation.
Article in Genes & development, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 101 citations in OpenAlex.
- Activation-derepression synergy enables a bHLH network to coordinate a signal-specific fate response.Cell reports · 2024Article
- Glycosyltransferase B4GALNT1 promotes immunosuppression in hepatocellular carcinoma via the HES4-SPP1-TAM/Th2 axis.Molecular biomedicine · 2024Article
- Mechanisms of Binding Specificity among bHLH Transcription Factors.International journal of molecular sciences · 2021Review
- Nerve Growth Factor Stimulates Glioblastoma Proliferation through Notch1 Receptor Signaling.Journal of Korean Neurosurgical Society · 2018Article
- Notch-mediated lateral inhibition is an evolutionarily conserved mechanism patterning the ectoderm in echinoids.Development genes and evolution · 2018Article
- Neuroblast differentiation during development and in neuroblastoma requires KIF1Bβ-mediated transport of TRKA.Genes & development · 2017Article
- Hes1: the maestro in neurogenesis.Cellular and molecular life sciences : CMLS · 2016Review
- The transcriptional repressor Hes1 attenuates inflammation by regulating transcription elongation.Nature immunology · 2016Article
- Transcription factor Hes1 modulates osteoarthritis development in cooperation with calcium/calmodulin-dependent protein kinase 2.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Adoptive transfer of heme oxygenase-1 (HO-1)-modified macrophages rescues the nuclear factor erythroid 2-related factor (Nrf2) antiinflammatory phenotype in liver ischemia/reperfusion injury.Molecular medicine (Cambridge, Mass.) · 2014Article
- Hes-1 SUMOylation by protein inhibitor of activated STAT1 enhances the suppressing effect of Hes-1 on GADD45α expression to increase cell survival.Journal of biomedical science · 2014Article
- Exposure to 1800 MHz radiofrequency radiation impairs neurite outgrowth of embryonic neural stem cells.Scientific reports · 2014Article
- Collier/OLF/EBF-dependent transcriptional dynamics control pharyngeal muscle specification from primed cardiopharyngeal progenitors.Developmental cell · 2014Article
- HES1 is a master regulator of glucocorticoid receptor-dependent gene expression.Science signaling · 2013Article
- JNK1 inhibits GluR1 expression and GluR1-mediated calcium influx through phosphorylation and stabilization of Hes-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Human homolog of Drosophila Hairy and enhancer of split 1, Hes1, negatively regulates δ-catenin (CTNND2) expression in cooperation with E2F1 in prostate cancer.Molecular cancer · 2010Article
- Article
- Progenitor cell proliferation in the retina is dependent on Notch-independent Sonic hedgehog/Hes1 activity.The Journal of cell biology · 2009Article
- Hes-6, an inhibitor of Hes-1, is regulated by 17beta-estradiol and promotes breast cancer cell proliferation.Breast cancer research : BCR · 2009Article
- Repression of chondrogenesis through binding of notch signaling proteins HES-1 and HEY-1 to N-box domains in the COL2A1 enhancer site.Arthritis and rheumatism · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The induction of neurite outgrowth by NGF is a transcription-dependent process in PC12 cells, but the transcription factors that mediate this process are not known. Here we show that the bHLH transcriptional repressor HES-1 is a mediator of this process. Inactivation of endogenous HES-1 by forced expression of a dominant-negative protein induces neurite outgrowth in the absence of NGF and increases response to NGF. In contrast, expression of additional wild-type HES-1 protein represses and delays response to NGF. Endogenous HES-1 DNA-binding activity is post-translationally inhibited during NGF signaling in vivo, and phosphorylation of PKC consensus sites in the HES-1 DNA-binding domain inhibits DNA binding by purified HES-1 in vitro. Mutation of these sites generates a constitutively active protein that strongly and persistently blocks response to NGF. These results suggest that post-translational inhibition of HES-1 is both essential for and partially mediates the induction of neurite outgrowth by NGF signaling.
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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.