ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
A dominant negative Egr inhibitor blocks nerve growth factor-induced neurite outgrowth by suppressing c-Jun activation: role of an Egr/c-Jun complex.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 69 citations in OpenAlex.
- Midnolin, a Genetic Risk Factor for Parkinson's Disease, Promotes Neurite Outgrowth Accompanied by Early Growth Response 1 Activation in PC12 Cells.Molecular and cellular biology · 2024Article
- Early Growth Response Gene Upregulation in Epstein-Barr Virus (EBV)-Associated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).Biomolecules · 2020Review
- Review
- Robust gene expression programs underlie recurrent cell states and phenotype switching in melanoma.Nature cell biology · 2020Article
- Protein-protein interactions underlying the behavioral and psychological symptoms of dementia (BPSD) and Alzheimer's disease.PloS one · 2020Article
- The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders.Frontiers in behavioral neuroscience · 2017Review
- Boolean Modeling Reveals the Necessity of Transcriptional Regulation for Bistability in PC12 Cell Differentiation.Frontiers in genetics · 2016Article
- The estrous cycle surpasses sex differences in regulating the transcriptome in the rat medial prefrontal cortex and reveals an underlying role of early growth response 1.Genome biology · 2015Article
- Involvement of IKAP in peripheral target innervation and in specific JNK and NGF signaling in developing PNS neurons.PloS one · 2014Article
- Transcriptional Regulation of EGR1 by EGF and the ERK Signaling Pathway in Prostate Cancer Cells.Genes & cancer · 2011Article
- Functional whole-genome analysis identifies Polo-like kinase 2 and poliovirus receptor as essential for neuronal differentiation upstream of the negative regulator alphaB-crystallin.The Journal of biological chemistry · 2009Article
- Expression profiling and Ingenuity biological function analyses of interleukin-6- versus nerve growth factor-stimulated PC12 cells.BMC genomics · 2009Article
- Short-term striatal gene expression responses to brain-derived neurotrophic factor are dependent on MEK and ERK activation.PloS one · 2009Article
- A cAMP-dependent, protein kinase A-independent signaling pathway mediating neuritogenesis through Egr1 in PC12 cells.Molecular pharmacology · 2008Article
- Regulation of rat dopamine beta-hydroxylase gene transcription by early growth response gene 1 (Egr1).Brain research · 2008Article
- Rat Urinary Bladder Carcinogenesis by Dual-Acting PPARalpha + gamma Agonists.PPAR research · 2008Article
- Hippocampal expression analyses reveal selective association of immediate-early, neuroenergetic, and myelinogenic pathways with cognitive impairment in aged rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Expression profiling upon Nex1/MATH-2-mediated neuritogenesis in PC12 cells and its implication in regeneration.Journal of neurochemistry · 2004Article
- ERK activation promotes neuronal degeneration predominantly through plasma membrane damage and independently of caspase-3.The Journal of cell biology · 2004Article
- BMP enhances transcriptional responses to NGF during PC12 cell differentiation.Neurochemical researchArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the Egr family of transcription factors are rapidly and robustly induced by neurotransmitters and neurotrophins and have been implicated in mediating enduring changes in neuronal function elicited by these stimuli. Because we have found in previous studies that a dominant negative inhibitor of Egr action, the Egr zinc finger domain (ZnEgr), blocks NGF-induced neurite outgrowth in PC12 cells, we have used this preparation to help identify the downstream targets of Egr proteins involved in plasticity. Our investigation into the mechanism of action of ZnEgr indicates that it blocks NGF-induced neurite outgrowth by suppressing activation of c-Jun, a critical step in the signaling pathway mediating this response. Although we had assumed that ZnEgr exerts its effects by binding to the Egr response element (ERE) and thereby blocking target gene regulation by Egr proteins, this classical mode of action appears to be too slow to mediate the effects of Egr proteins on c-Jun activation. In evaluating alternative ERE-independent mechanisms of Egr (and ZnEgr) action, we found that Egr1 and c-Jun coprecipitate and that ZnEgr disrupts formation of the Egr1/c-Jun complex. Furthermore, mutations of ZnEgr that greatly impair or abolish its ability to bind to the ERE do not block its ability to suppress c-Jun activation or neurite outgrowth induced by NGF. Accordingly, our studies indicate that Egr and ZnEgr proteins regulate c-Jun activation via a novel mechanism, protein-protein interaction with c-Jun, rather than via their classical mode of action, binding to the ERE.
Indexed as
Identifiers
12019303PMC6757642W2116236374What Socratic holds
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 Socratic graph.