ArticleMolecular biology of the cell2004
The dynamic association of RCC1 with chromatin is modulated by Ran-dependent nuclear transport.
Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Methods to separate nuclear soluble fractions reflecting localizations in living cells.iScience · 2021Article
- Disruption of the ran system by cysteine oxidation of the nucleotide exchange factor RCC1.Molecular and cellular biology · 2015Article
- Influenza virus ribonucleoprotein complexes gain preferential access to cellular export machinery through chromatin targeting.PLoS pathogens · 2011Article
- The methylated N-terminal tail of RCC1 is required for stabilisation of its interaction with chromatin by Ran in live cells.BMC cell biology · 2010Article
- Quantitative analysis of chromatin compaction in living cells using FLIM-FRET.The Journal of cell biology · 2009Article
- Functionalization of a nanopore: the nuclear pore complex paradigm.Biochimica et biophysica acta · 2009Review
- Apoptotic histone modification inhibits nuclear transport by regulating RCC1.Nature cell biology · 2009Article
- Functional analysis of key nuclear trafficking components reveals an atypical Ran network required for parasite pathogenesis.Molecular microbiology · 2008Article
- BMAL1 shuttling controls transactivation and degradation of the CLOCK/BMAL1 heterodimer.Molecular and cellular biology · 2006Article
- Regulation of the EBNA1 Epstein-Barr virus protein by serine phosphorylation and arginine methylation.Journal of virology · 2006Article
- Dissecting the contribution of diffusion and interactions to the mobility of nuclear proteins.Biophysical journal · 2006Article
- Nuclear localization and dynamic properties of the Marek's disease virus oncogene products Meq and Meq/vIL8.Journal of virology · 2006Article
- The mobile nucleoporin Nup2p and chromatin-bound Prp20p function in endogenous NPC-mediated transcriptional control.The Journal of cell biology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Regulator of chromosome condensation (RCC1) binding to chromatin is highly dynamic, as determined by fluorescence recovery after photobleaching analysis of GFP-RCC1 in stably transfected tsBN2 cells. Microinjection of wild-type or Q69L Ran markedly slowed the mobility of GFP-RCC1, whereas T24N Ran (defective in nucleotide loading) decreased it further still. We found significant alterations in the mobility of intranuclear GFP-RCC1 after treatment with agents that disrupt different Ran-dependent nuclear export pathways. Leptomycin B, which inhibits Crm1/RanGTP-dependent nuclear export, significantly increased the mobility of RCC1 as did high levels of actinomycin D (to inhibit RNA polymerases I, II, and III) or alpha-amanitin (to inhibit RNA polymerases II and III) as well as energy depletion. Inhibition of just mRNA transcription, however, had no affect on GFP-RCC1 mobility consistent with mRNA export being a Ran-independent process. In permeabilized cells, cytosol and GTP were required for the efficient release of GFP-RCC1 from chromatin. Recombinant Ran would not substitute for cytosol, and high levels of supplemental Ran inhibited the cytosol-stimulated release. Thus, RCC1 release from chromatin in vitro requires a factor(s) distinct from, or in addition to, Ran and seems linked in vivo to the availability of Ran-dependent transport cargo.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.