id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-013840-mi3uf4vk	Zhang, Wei	The metabolic regulator Lamtor5 suppresses inflammatory signaling via regulating mTOR-mediated TLR4 degradation	2019-08-29		.txt	text/plain	8495	495	43	Specifically, Lamtor5 associated with TLR4 via their LZ/TIR domains and facilitated their colocalization at autolysosomes, preventing lysosomal tethering and the activation of mTORC1 upon LPS stimulation and thereby derepressing TFEB to promote autophagic degradation of TLR4. 16, 17 Loss of the autophagic components autophagy-related 16 like 1, Beclin1, and microtubule-associated protein 1A/1B light chain 3 (LC3) enhanced the macrophage response to LPS, a prototypical agonist of TLR4, and caused sustained inflammatory signaling. [26] [27] [28] A recent study identified Lamtor5 as an indispensable component of the Ragulator complex that interacts with small GTPase Ras-related GTP binding protein (RAG), contributing to lysosomal recruitment and the activation of mechanistic target of rapamycin complex 1 (mTORC1) in response to amino acids. j Immunoblotting for TLR4 and total and phosphorylated p65 in control and Lamtor5-expressing RAW264.7 cells pretreated with DMSO or Baf1 and then stimulated with LPS for the indicated time periods.	./cache/cord-013840-mi3uf4vk.txt	./txt/cord-013840-mi3uf4vk.txt