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Nuclear export of TIS11 (show ZFP36 Proteins) proteins is mediated by CRM1 through diverging nuclear export signals, while their nuclear import mechanism may rely on a highly conserved signal whose activity is negatively regulated by ZnF2 (show ZNF2 Proteins) folding.
HPO (show GFER Proteins) promotes the translocation of SD to the cytoplasm in a CRM1-dependent manner
Exportin-1 is a nuclear export receptor for expanded polyQ containing proteins.
Nuclear localization of the ecdysteroid receptor (EcR) is increased in HeLa cells if exportin-1 (CRM1) is knocked down by siRNA against exportin.
Data show that downregulation of YAN involves CRM1-mediated nuclear export, and that MAE is involved in MAPK (show MAPK1 Proteins) phosphorylationof YAN.
A major function of DNup88 is to anchor DNup214 and CRM1 on the nuclear envelope and thereby attenuate NES (show NES Proteins)-mediated nuclear export.
Phosphorylation of Yan favors Crm1 in this competition and counteracts inhibition of nuclear export by Mae
two functional nuclear export signals are in the Sima basic helix-loop-helix (bHLH) domain and promote CRM1-dependent nuclear export
We describe three in vitro reconstituted disassembly intermediates, which show binding of a Crm1 export complex via two FG-repeat patches, cargo-release by RanBP2's Ran-binding domains and retention of free Crm1 at RanBP2 after Ran-GTP (show AK3 Proteins) hydrolysis.
Nuclear entrapment of p33ING1b (show ING1 Proteins) by inhibition of exportin-1 triggers apoptosis in head and neck squamous cell cancer cells.
CDK4 (show CDK4 Proteins) and XPO1 are not altered in a rare undifferentiated sarcoma, making them therapeutic targets
The subcellular distributions of IkappaB and NFkappaB are indicative of carcinogenesis. Inhibition of XPO1 results in intranuclear retention of IkappaB, which inhibits NFkappaB and thereby provides a novel mechanism for drug therapy in sarcoma. This effect can be further enhanced in relatively selinexor-resistant sarcoma cell lines by pretreatment with the proteasome inhibitor carfilzomib.
this work advocates for assessing 2p+ and XPO1 mutations before choosing a chronic lymphocytic leukemia therapy.
Importin-beta and CRM1 control a RANBP2 spatiotemporal switch essential for mitotic kinetochore function.
We provide evidence for a regulatory role of CRM1 (chromosome-region-maintenance-1; also known as XPO1, exportin-1) in juxta-nuclear microtubule-dependent adenovirus transport. Leptomycin B (LMB) abolishes nuclear targeting of adenovirus. It binds to CRM1, precludes CRM1-cargo binding and blocks signal-dependent nuclear export.
in leukemia cell lines an XPO1 heterozygous mutation confers similar resistance against selinexor as homozygous substitution, demonstrating that SINE resistance can be obtained by a single and dominant mutation of the cysteine528 residue in XPO1
XPO1 inhibitor combination therapy with bortezomib or carfilzomib induces nuclear localization of IkappaBalpha (show NFKBIA Proteins) and overcomes acquired proteasome inhibitor resistance in human multiple myeloma.
KPT-8602 is highly specific for XPO1 inhibition and demonstrates potent anti-leukemic activity supporting clinical application of the second-generation SINE compound for the treatment of Acute Lymphoblastic Leukemia
CRM1 binds to Axin (show AXIN1 Proteins) in the presence of RanGTP
These results suggest a differential interaction between human Crm1 and mouse Crm1 and many lentiviral Rev proteins, which may partially explain the HIV replicative defect in mice.
Data show that administration of a single dose of selinexor bound Exportin 1 (XPO1/CRM1) for minimally 72 hours both in vitro and in vivo.
These results suggest a model wherein HIV-1 Rev-associated nuclear export signals cooperate to regulate the number or quality of CRM1's interactions with viral Rev/RRE ribonucleoprotein complexes in the nucleus.
map the nuclear import and export signals of Dp71d by truncation and point mutant analysis, showing for the first time Dp71d shuttles between nucleus and cytoplasm mediated by conventional nuclear transporters, importin (IMP (show BRAP Proteins)) alpha/beta and the exportin CRM1
AKT3 (show AKT3 Proteins) controls mitochondrial biogenesis and autophagy via regulation of the major nuclear export protein CRM-1.
A CRM1-mediated nuclear export signal is essential for cytoplasmic localization of neurogenin 3 (show NEUROG3 Proteins) in neurons.
Bioavailable CRM1 inhibitor KPT-251 significantly inhibited renal cell carcinoma (show MOK Proteins) growth in vivo with the expected on target effects and no obvious toxicity.
CRM1 augments production of infectious human and feline immunodeficiency viruses from murine cells
CaMKI (show CAMK1 Proteins) vies with CRM1/exportin 1 for access to a nuclear export signal, and assembly of a CaMKI (show CAMK1 Proteins)-14-3-3 zeta (show YWHAZ Proteins)-CCTalpha (show PCYT1A Proteins) complex is a key effector mechanism that drives nuclear CCTalpha (show PCYT1A Proteins) translocation.
Transcription-independent role of Bach1 (show BACH1 Proteins) in mitosis through a nuclear exporter Crm1-dependent mechanism.
The protein encoded by this gene mediates leucine-rich nuclear export signal (NES)-dependent protein transport. Exportin 1 specifically inhibits the nuclear export of Rev and U snRNAs. It is involved in the control of several cellular processes by controlling the localization of cyclin B, MPAK, and MAPKAP kinase 2. This protein also regulates NFAT and AP-1.
, chromosomal region maintenance 1
, exportin 1
, exportin 1 (CRM1 homolog, yeast)
, exportin 1-like
, CRM1, yeast, homolog
, chromosome region maintenance 1 protein homolog
, exportin 1 (CRM1, yeast, homolog)
, exportin-1 (required for chromosome region maintenance)
, nuclear export factor CRM1
, CRM1/XPO1 protein