ArticleJournal of cell science2009
Repression of classical nuclear export by S-nitrosylation of CRM1.
Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 53 citations in OpenAlex.
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- SINE compounds activate exportin 1 degradation through an allosteric mechanism.Nature chemical biology · 2025Article
- Signal amplification in the KEAP1-NRF2-ARE antioxidant response pathway.Redox biology · 2022Review
- Karyopherin-mediated nucleocytoplasmic transport.Nature reviews. Molecular cell biology · 2022Review
- Precision Redox: The Key for Antioxidant Pharmacology.Antioxidants & redox signaling · 2021Review
- Nucleocytoplasmic Transport: Regulatory Mechanisms and the Implications in Neurodegeneration.International journal of molecular sciences · 2021Review
- Protein S-nitrosylation regulates proteostasis and viability of hematopoietic stem cell during regeneration.Cell reports · 2021Article
- Nitrosative stress inhibits aminoacylation and editing activities of mitochondrial threonyl-tRNA synthetase by S-nitrosation.Nucleic acids research · 2020Article
- Cytoplasmic, but not nuclear Nrf2 expression, is associated with inferior survival and relapse rate and response to platinum-based chemotherapy in non-small cell lung cancer.Thoracic cancer · 2020Article
- S-Nitrosylation: An Emerging Paradigm of Redox Signaling.Antioxidants (Basel, Switzerland) · 2019Review
- The coming-of-age of nucleocytoplasmic transport in motor neuron disease and neurodegeneration.Cellular and molecular life sciences : CMLS · 2019Review
- Developmental Alcohol Exposure Impairs Activity-Dependent S-Nitrosylation of NDEL1 for Neuronal Maturation.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Visualization of aging-associated chromatin alterations with an engineered TALE system.Cell research · 2017Article
- Extensive cargo identification reveals distinct biological roles of the 12 importin pathways.eLife · 2017Article
- Quantitative Proteomics Analysis of VEGF-Responsive Endothelial Protein S-Nitrosylation Using Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC) and LC-MS/MS.Biology of reproduction · 2016Article
- Redox control of microglial function: molecular mechanisms and functional significance.Antioxidants & redox signaling · 2014Review
- Thiol-based redox proteins in abscisic acid and methyl jasmonate signaling in Brassica napus guard cells.The Plant journal : for cell and molecular biology · 2014Article
- Article
- Thioredoxin Interacting Protein (TXNIP) and Pathogenesis of Diabetic Retinopathy.Journal of clinical & experimental ophthalmology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The karyopherin chromosomal region maintenance 1 (CRM1) is the major receptor for classical nuclear protein export. However, little is known about the regulation of CRM1 itself. Here, we report that cellular CRM1 became S-nitrosylated after extensive exposure to endogenous or exogenous nitric oxide (NO). This abrogated the interaction of CRM1 with nuclear export signals (NESs) and repressed classical protein export. Analysis by mass spectrometry and involving the use of S-nitrosylation mimetic mutations indicated that modification at either of two specific cysteines of CRM1 was sufficient to abolish the CRM1-NES association. Moreover, ectopic overexpression of the corresponding S-nitrosylation-resistant CRM1 mutants rescued NO-induced repression of nuclear export. We also found that inactivation of CRM1 by NO facilitated the nuclear accumulation of the antioxidant response transcription factor Nrf2 and transcriptional activation of Nrf2-controlled genes. Together, these data demonstrate that CRM1 is negatively regulated by S-nitrosylation under nitrosative stress. We speculate that this is important for promoting a cytoprotective transcriptional response to nitrosative stress.
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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.