3 nuclear transport disease
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Q: What is the function of the HIV Rev protein?
A: It binds the RRE and exports unspliced or partially spliced HIV RNA.
Q: Where is the RRE located?
A: On an RNA structure within an intron of HIV RNA.
Q: What signal allows Rev to enter the nucleus?
A: A Nuclear Localization Signal (NLS).
Q: What method was used to study Rev export in Xenopus oocytes?
A: Nuclear microinjection followed by nuclear/cytoplasmic fractionation.
Q: What did the Xenopus assay show about Rev export?
A: Rev moves from the nucleus to the cytoplasm over time.
Q: What does Leptomycin B inhibit?
A: CRM1/exportin-1.
Q: How does LMB affect Rev nuclear export?
A: It blocks Rev export
Q: Does LMB affect importin-α export?
A: No
Q: What motif does Rev use to bind CRM1?
A: A leucine-rich Nuclear Export Signal (NES).
Q: What technique demonstrated direct binding between Rev NES and CRM1?
A: Yeast two-hybrid assay.
Q: What happens when the leucines in the Rev NES are mutated?
A: CRM1 binding is abolished.
Q: What conformational change allows CRM1 to bind NES cargo?
A: Ran-GTP binding opens the hydrophobic NES-binding cleft.
Q: How does LMB inhibit CRM1 at the molecular level?
A: It covalently modifies Cys528 in the NES-binding groove.
Q: Why is CRM1 a target in cancer therapy?
A: Overactive CRM1 exports tumor suppressors
Q: What are SINE compounds?
A: Selective Inhibitors of Nuclear Export designed to inhibit CRM1 with less toxicity.
Q: What is the FDA-approved CRM1 inhibitor?
A: Selinexor (KPT-330).
Q: What mutation confers resistance to CRM1 inhibitors?
A: CRM1 Cys528 mutation.
Q: Where is NFAT located at resting calcium levels?
A: In the cytoplasm.
Q: What causes NFAT to enter the nucleus?
A: Increased calcium activates calcineurin
Q: How does phosphorylation affect NFAT localization?
A: Phosphorylated → cytoplasm; dephosphorylated → nucleus.
Q: Which drugs inhibit NFAT nuclear import?
A: Calcineurin inhibitors (e.g.
Q: What genetic mutation causes ALS/FTD?
A: G4C2 repeat expansion in C9orf72.
Q: What organism was used to model C9orf72 toxicity?
A: Drosophila.
Q: How does increasing repeat length affect Drosophila eyes?
A: Longer repeats cause severe degeneration.
Q: What pathway repeatedly modifies repeat toxicity?
A: Nucleocytoplasmic transport (Ran/RanGAP pathway).
Q: What happens to Ran localization in disease models?
A: Ran becomes mislocalized from nucleus to cytoplasm.
Q: What effect does RanGAP overexpression have?
A: It rescues toxicity and reduces degeneration.
Q: What structure does expanded G4C2 RNA form?
A: RNA G-quadruplexes.
Q: How do G-quadruplexes disrupt transport?
A: They bind/sequester RanGAP
Q: What additional toxic products come from the repeat?
A: Dipeptide repeat proteins via RAN translation.
Q: What are the two main mechanisms of C9orf72 toxicity?
A: RNA-mediated sequestration of transport factors and dipeptide repeat protein toxicity.
Note 
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