ArticleJournal of neurochemistry2008
Rit signaling contributes to interferon-gamma-induced dendritic retraction via p38 mitogen-activated protein kinase activation.
Article in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Amyloid-β Pathology-Specific Cytokine Secretion Suppresses Neuronal Mitochondrial Metabolism.Cellular and molecular bioengineering · 2023Article
- A single-cell atlas reveals the heterogeneity of meningeal immunity in a mouse model of Methyl CpG binding protein 2 deficiency.Frontiers in immunology · 2022Article
- The molecular functions of RIT1 and its contribution to human disease.The Biochemical journal · 2020Review
- RIT1 suppresses esophageal squamous cell carcinoma growth and metastasis and predicts good prognosis.Cell death & disease · 2018Article
- RIT1 controls actin dynamics via complex formation with RAC1/CDC42 and PAK1.PLoS genetics · 2018Article
- Reversible nerve damage and corneal pathology in murine herpes simplex stromal keratitis.Journal of virology · 2014Article
- Maternal immune activation leads to activated inflammatory macrophages in offspring.Brain, behavior, and immunity · 2014Article
- Rit subfamily small GTPases: regulators in neuronal differentiation and survival.Cellular signalling · 2013Review
- Putting the Rit in cellular resistance: Rit, p38 MAPK and oxidative stress.Communicative & integrative biology · 2013Article
- Rit GTPase regulates a p38 MAPK-dependent neuronal survival pathway.Neuroscience letters · 2012Article
- Rit-mediated stress resistance involves a p38-mitogen- and stress-activated protein kinase 1 (MSK1)-dependent cAMP response element-binding protein (CREB) activation cascade.The Journal of biological chemistry · 2012Article
- An evolutionarily conserved Rit GTPase-p38 MAPK signaling pathway mediates oxidative stress resistance.Molecular biology of the cell · 2011Article
- Ras family small GTPase-mediated neuroprotective signaling in stroke.Central nervous system agents in medicinal chemistry · 2011Review
- A rit GTPase-p38 mitogen-activated protein kinase survival pathway confers resistance to cellular stress.Molecular and cellular biology · 2011Article
- Src-dependent TrkA transactivation is required for pituitary adenylate cyclase-activating polypeptide 38-mediated Rit activation and neuronal differentiation.Molecular biology of the cell · 2010Article
- Cytokine dysregulation in autism spectrum disorders (ASD): possible role of the environment.Neurotoxicology and teratologyReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The proinflammatory cytokine interferon-gamma (IFNgamma) alters neuronal connectivity via selective regressive effects on dendrites but the signaling pathways that mediate this effect are poorly understood. We recently demonstrated that signaling by Rit, a member of the Ras family of GTPases, modulates dendritic growth in primary cultures of sympathetic and hippocampal neurons. In this study, we investigated a role for Rit signaling in IFNgamma-induced dendritic retraction. Expression of a dominant negative Rit mutant inhibited IFNgamma-induced dendritic retraction in cultured embryonic rat sympathetic and hippocampal neurons. In pheochromacytoma cells and hippocampal neurons, IFNgamma caused rapid Rit activation as indicated by increased GTP binding to Rit. Silencing of Rit by RNA interference suppressed IFNgamma-elicited activation of p38 MAPK in pheochromacytoma cells, and pharmacological inhibition of p38 MAPK significantly attenuated the dendrite-inhibiting effects of IFNgamma in cultured sympathetic and hippocampal neurons without altering signal transducer and activator of transcription 1 activation. These observations identify Rit as a downstream target of IFNgamma and suggest that a novel IFNgamma-Rit-p38 signaling pathway contributes to dendritic retraction and may, therefore, represent a potential therapeutic target in diseases with a significant neuroinflammatory component.
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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.