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IKKbeta is required for the formation of the NLRP3 inflammasome

ABSTRACT: The rapid formation and activation of the NLRP3 inflammasome is induced by co-stimulation with LPS and nigericin. It requires the LPS-stimulated activation of IKK which exerts its effects independently of de novo gene transcription, protein translation and other protein kinases activated by IKK. IKK is not required for the nigericin-induced dispersion of the trans-Golgi network (TGN), but to bring NLRP3 in proximity with TGN38. The nigericin induced dispersion of the Golgi is enhanced by co-stimulation with LPS, and this enhancement is IKK-dependent. Prolonged stimulation with LPS to increase the expression of NLRP3, followed by stimulation with nigericin, produced larger TGN38-positive puncta, and the ensuing activation of the NLRP3 inflammasome was also suppressed by IKK inhibitors added prior to stimulation with nigericin. IKK therefore has a key role in recruiting NLRP3 to the dispersed TGN, leading to the formation and activation of the NLRP3 inflammasome.

SUBMITTER: Dr. Sambit, Kumar Nanda

PROVIDER: S-SCDT-EMBOR-2020-50743V1 | biostudies-other |

REPOSITORIES: biostudies-other

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IKKβ is required for the formation of the NLRP3 inflammasome.

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| S-SCDT-10_15252-EMBJ_2023113481 | biostudies-other

MARCH5-dependent NLRP3 ubiquitination is required for mitochondrial NLRP3-NEK7 complex formation and NLRP3 inflammasome activation.

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The NLRP3 Inflammasome Is Required for Protection Against Pseudomonas Keratitis.

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