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. 2019 Jul 19;17(7):e3000382. doi: 10.1371/journal.pbio.3000382

Fig 7. LATS1/2 restrict NFκB to maintain epithelial identity and coordinate proliferation and differentiation of pancreatic progenitors.

Fig 7

(A) During embryonic development, LATS1/2 kinases exquisitely control subcellular localization of YAP1/TAZ, thereby maintaining pancreas progenitors and coordinating morphogenesis, cell proliferation. NFκB TFs also shuttle between the nucleus and cytoplasm, depending on activation, and coordinate cell proliferation. (B) Lats1/2 deficiency triggers NFκB activators like VNN1, a pantetheinase enzyme that converts pantetheine to pantothenic acid and cysteamine. VNN1 products increase ROS and activate NFκB, leading to initiation of EMT and mesenchymal gene expression. EMT, epithelial-mesenchymal transition; LATS1/2, large tumor suppressor kinases 1 and 2; NFκB, nuclear factor kappa light chain enhancer of activated B cells; ROS, reactive oxygen species; TAZ, transcriptional coactivator with PDZ-binding motif; TF, transcription factor; VNN1, vanin1; YAP1, yes-associated protein 1.