ppat.1010478.g002.tif (778.33 kB)
PLOD1 shRNA depletion and small molecule inhibition with 2-DP destabilize EBNA1 protein.
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posted on 2023-06-01, 17:32 authored by Jayaraju Dheekollu, Andreas Wiedmer, Samantha S. Soldan, Leonardo Josué Castro- Muñoz, Christopher Chen, Hsin-Yao Tang, David W. Speicher, Paul M. LiebermanA) Raji cells transduced with lentivirus shControl (shCtrl) or shPLOD1 (pool a) were assayed by Western blot for PLOD1, EBNA1, EBNA2, LMP1, or Actin at 7 days post-transduction. Each lane is a biological replicate. B) Raji (left) or LCL (right) treated with DMSO or 2,’2-dipyridil (2-DP, 200 μM) were assayed by Western blot for PLOD1, EBNA1, EBNA2, LMP1, or Actin. C) Raji (left) or LCL (right) were treated with DMSO, 2-DP (200 μM), 2-DP+MG132 (10 μM), or 17-DMGA (1 μM) for 48 hrs and assayed by Western blot for EBNA1 (top) or Actin (bottom). D) Raji (left) or LCL (right) were treated with DMSO, 2-DP (200 μM), or CoCl2 (100 μM) for 48 hrs followed by Western blot for PLOD1, EBNA1, HIF1α, or Actin.
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ubiquitous human γnovel interaction partnerhighly stable proteinpositive lymphoid cellslatently infected cellsebna1 revealed interactionebna1 protein stabilityebna1 protein levelsdriven dna replicationdna replication activityk461 perturbed interactionsviral plasmid replicationselective growth inhibitiondiv >< pk461 abrogates ebna1viral episome maintenancedna replicationepisome maintenanceproliferating cellsvarious malignanciesproteomic analysisprocollagen lysineorip lysine hydroxylationlatent infectionfully understoodfindings suggestebna1 functioncausally associatedbarr virusautoimmune disease
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