SINT speckles are membraneless cytosolic speckles formed in response to cellular stress. SINT speckles partially colocalize with active TBK1, and TBK1 phosphorylation is reduced when SINTBAD and the SINT speckle component AZI2 are deleted. The acetyltransferase KAT2A (GCN5) regulates the dynamic production of SINT speckles, which is inhibited by heat shock protein-mediated chaperone action. The autophagy-initiating kinases ULK1/2 also suppress SINT speckle formation, and knocking these kinases out prevented focal TBK1 phosphorylation in a pathway-specific manner (31442668).
Saul VV, Seibert M, Krüger M, Jeratsch S, Kracht M, Schmitz ML. ULK1/2 Restricts the Formation of Inducible SINT-Speckles, Membraneless Organelles Controlling the Threshold of TBK1 Activation. iScience. 2019 Sep 27;19:527-544. doi: 10.1016/j.isci.2019.08.001. Epub 2019 Aug 6. PMID: 31442668; PMCID: PMC6710720.