Gating Immunity and Death at the Nuclear Pore Complex

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Gating Immunity and Death at the Nuclear Pore Complex Mary Dasso, Beatriz M.A. Fontoura Cell Volume 166, Issue 6, Pages 1364-1366 (September 2016) DOI: 10.1016/j.cell.2016.08.026 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 Nuclear Pore Rearrangement upon NB-LRR Signaling Induces Effector-Triggered Immunity and Programmed Cell Death The activation of nucleotide-binding leucine-rich repeat receptor proteins (NB-LRR) results in disruption of CPR5 oligomerization, which causes the release of cyclin-dependent kinase inhibitors (CKIs) sequestered by CPR5 and rearrangement of trafficking through the nuclear pore complex. Together, these effects cause immune/stress signaling cargos to enter the nucleus to trigger transcription of genes that encode proteins that function in effector-triggered immunity (ETI) and programmed cell death (PCD). Cell 2016 166, 1364-1366DOI: (10.1016/j.cell.2016.08.026) Copyright © 2016 Elsevier Inc. Terms and Conditions