ArticleCellular and molecular life sciences : CMLS2016
A cellular reporter to evaluate CRM1 nuclear export activity: functional analysis of the cancer-related mutant E571K.
Article in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting Exportin-1 in Cancer: From Nuclear Export to Oncogenic Transcriptional Hubs.JMA journal · 2026Review
- XPO1/Exportin-1 in Acute Myelogenous Leukemia; Biology and Therapeutic Targeting.Biomolecules · 2025Review
- Modulation of anti-tumour immunity by XPO1 inhibitors.Exploration of targeted anti-tumor therapy · 2025Review
- Prognostic and functional role of the nuclear export receptor 1 (XPO1) in gastrointestinal cancers: a potential novel target?Molecular biology reports · 2024Review
- Mutations of Key Functional Residues in CRM1/XPO1 Differently Alter Its Intranuclear Localization and the Nuclear Export of Endogenous Cargos.Biomolecules · 2024Article
- The nuclear export protein exportin-1 in solid malignant tumours: From biology to clinical trials.Clinical and translational medicine · 2024Review
- Exportin 1-mediated nuclear/cytoplasmic trafficking controls drug sensitivity of classical Hodgkin's lymphoma.Molecular oncology · 2023Article
- Nuclear transport proteins: structure, function, and disease relevance.Signal transduction and targeted therapy · 2023Review
- Karyopherin-mediated nucleocytoplasmic transport.Nature reviews. Molecular cell biology · 2022Review
- Distinct genomic landscape of Chinese pediatric acute myeloid leukemia impacts clinical risk classification.Nature communications · 2022Article
- Selective Disruption of Survivin's Protein-Protein Interactions: A Supramolecular Approach Based on Guanidiniocarbonylpyrrole.Chembiochem : a European journal of chemical biology · 2022Article
- Impact of XPO1 mutations on survival outcomes in metastatic non-small cell lung cancer (NSCLC).Lung cancer (Amsterdam, Netherlands) · 2021Article
- Specific inhibition of the Survivin-CRM1 interaction by peptide-modified molecular tweezers.Nature communications · 2021Article
- The nuclear export protein XPO1 - from biology to targeted therapy.Nature reviews. Clinical oncology · 2021Review
- Article
- Using a Simple Cellular Assay to Map NES Motifs in Cancer-Related Proteins, Gain Insight into CRM1-Mediated NES Export, and Search for NES-Harboring Micropeptides.International journal of molecular sciences · 2020Article
- Inhibition of chromosomal region maintenance 1 suppresses the migration and invasion of glioma cells via inactivation of the STAT3/MMP2 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- Small Molecule Inhibitors of CRM1.Frontiers in pharmacology · 2020Review
- Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis.Cancer discovery · 2019Article
- The past, present, and future of CRM1/XPO1 inhibitors.Stem cell investigation · 2019Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The exportin CRM1 binds nuclear export signals (NESs), and mediates active transport of NES-bearing proteins from the nucleus to the cytoplasm. Structural and biochemical analyses have uncovered the molecular mechanisms underlying CRM1/NES interaction. CRM1 binds NESs through a hydrophobic cleft, whose open or closed conformation facilitates NES binding and release. Several cofactors allosterically modulate the conformation of the NES-binding cleft through intramolecular interactions involving an acidic loop and a C-terminal helix in CRM1. This current model of CRM1-mediated nuclear export has not yet been evaluated in a cellular setting. Here, we describe SRV100, a cellular reporter to interrogate CRM1 nuclear export activity. Using this novel tool, we provide evidence further validating the model of NES binding and release by CRM1. Furthermore, using both SRV100-based cellular assays and in vitro biochemical analyses, we investigate the functional consequences of a recurrent cancer-related mutation, which targets a residue near CRM1 NES-binding cleft. Our data indicate that this mutation does not necessarily abrogate the nuclear export activity of CRM1, but may increase its affinity for NES sequences bearing a more negatively charged C-terminal end.
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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.