GRASP55 and UPR control interleukin-1β aggregation and secretion

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dc.contributor.author	Chiritoiu, Marioara
dc.contributor.author	Brouwers, Nathalie
dc.contributor.author	Turacchio, Gabriele
dc.contributor.author	Pirozzi, Marianella
dc.contributor.author	Malhotra, Vivek
dc.date	2019
dc.identifier.citation	Chiritoiu M, Brouwers N, Turacchio G, Pirozzi M, Malhotra V. GRASP55 and UPR control interleukin-1β aggregation and secretion. Dev Cell. 2019; 49(1):145-155.e4. DOI 10.1016/j.devcel.2019.02.011
dc.identifier.citation	1534-5807
dc.identifier.citation	http://dx.doi.org/10.1016/j.devcel.2019.02.011
dc.identifier.uri	http://hdl.handle.net/10230/42195
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Elsevier
dc.relation	Dev Cell. 2019; 49(1):145-155.e4
dc.relation	info:eu-repo/grantAgreement/ES/1PE/BFU2013-44188-P
dc.relation	info:eu-repo/grantAgreement/ES/1PE/BFU2016_75372-P
dc.rights	info:eu-repo/semantics/embargoedAccess
dc.rights	© Elsevier http://dx.doi.org/10.1016/j.devcel.2019.02.011
dc.subject	GRASP
dc.subject	Interleukin-1β (IL-1β)
dc.subject	Unconventional protein secretion (UPS)
dc.subject	Unfolded protein response (UPR)
dc.title	GRASP55 and UPR control interleukin-1β aggregation and secretion
dc.type	info:eu-repo/semantics/article
dc.type	info:eu-repo/semantics/acceptedVersion
dc.description.abstract	Signal-sequence-lacking interleukin (IL)-1β, is cleaved by caspase-1 to mature mIL-1β, which is secreted, without entering the endoplasmic reticulum. We report that macrophages of GRASP55-/- mice are defective in mIL-1β secretion and retain it as intracellular aggregates. Intriguingly, GRASP55-/- macrophages are defective in the IRE1α branch of the unfolded protein response. This finding fits well with our data that inhibition of IRE1α also impairs mIL-1β secretion and causes its accumulation in intracellular aggregates. PERK inhibition, on the other hand, controls caspase-1-mediated conversion of proIL-1β to mIL-1β. These findings reveal translation-independent functions of PERK and IRE1α: PERK controls the production of mIL-1β, which is then followed by GRASP55 and IRE1α activity to keep mIL-1β in a secretion-competent form.
dc.description.abstract	This work was funded by grants from the Spanish Ministry of Economy and Competitiveness (BFU2013-44188-P and BFU2016_75372-P to V.M.). We acknowledge support of the Spanish Ministry of Economy and Competitiveness, through the Programmes “Centro de Excelencia Severo Ochoa 2013- 2017” (SEV-2012-0208 and SEV-2013-0347).

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