Disease relevance of Xpo1

• Epstein-Barr virus EB2 protein exports unspliced RNA via a Crm-1-independent pathway [1].
• A reporter vector developed from the 3' end of the MMTV provirus was Rem responsive and required both the presence of the MMTV env-U3 junction and a functional Crm1 pathway [2].

High impact information on Xpo1

• In contrast, La, which is a nuclear phosphoprotein, undergoes nucleocytoplasmic shuttling independent of the nuclear export protein Crm1 [3].
• Heme regulates gene expression by triggering Crm1-dependent nuclear export of Bach1 [4].
• These data indicate that in smooth muscle, stimulation of Ca2+-dependent, calcineurin-mediated nuclear import and suppression of Crm-1/JNK-dependent nuclear export are both required for induction of NFATc3 nuclear accumulation [5].
• The defect in production of MVMi ssDNA in fibroblasts can also be overcome by introducing a mutation in MVMi NS2 that enhances its interaction with Crm1 [6].
• Characterization of centrosomal association of nucleophosmin/B23 linked to Crm1 activity [7].

Biological context of Xpo1

• Complementary experimental approaches demonstrated that PLC-HDP family members are exported by the Crm1 pathway and contain an evolutionary conserved leucine-rich nuclear export signal [8].

Anatomical context of Xpo1

• Constitutively elevated nuclear export activity opposes Ca2+-dependent NFATc3 nuclear accumulation in vascular smooth muscle: role of JNK2 and Crm-1 [5].

Associations of Xpo1 with chemical compounds

• These data show that the nuclear export pathway used by steroid hormone receptors such as GR is distinct from the Crm1 pathway [9].
• The CLS directed leptomycin B-sensitive nuclear export of reporter proteins, suggesting its dependence on the nuclear exporter Crm1/exportin 1 [10].
• In Exp 2, the OB-LN difference of Exp 1 was decreased by giving naltrexone (10 mg/kg sc) before LiCl, which suggested opiate involvement [11].
• In Exp 1, healthy OB formed stronger CTAs than LN to a saccharin taste paired with lithium chloride (LiCl, 3 mEq/kg ip) [11].
• In Exp 1, following the oral IGF-I administration, serum IGF-I concentration increased at hour 4 (p<0.01) and returned to the hour 0 level by hour 8, whereas glucose concentration was lowest at hour 4 and returned to the hour 0 level by hour 16 [12].

References