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. 2021 Oct 11;17(15):4223–4237. doi: 10.7150/ijbs.64046

Figure 3.

Figure 3

Schematic examples of protein palmitoylation and metabolism, cancer, inflammation, neurodegeneration. a. In the model of non-alcoholic steatohepatitis (NASH), palmitate induces CD36 palmitoylation, and the enhanced palmitoylation promotes the CD36/Lyn/Fyn complex, impairs FA β-oxidation, causes lipid accumulation, increases inflammation and cytokines release. b. Transcriptional enhanced associate domain (TEAD) is autopalmitoylated and it could be affected by intracellular palmitate levels. Palmitoylation of TEAD is required for its association with YAP and the regulation of transcriptional output of Hippo signaling. c. The de novo synthesis of palmitate by FASN and CD36-mediated exogenous FA uptake are two important sources for MYD88palmitoylation, which is essential for IRAK4 recruitment, p38MAPK and p65 activation, TLR4/MYD88 pathway. d. Palmitate deposition in the hippocampus increases GluA1 palmitoylation through FoxO3a-mediated overexpression of zDHHC3, resulting in altered GluA1 localization and function, suppressed AMPAR response and impairment of cognitive function. Figures include data from references 62, 41, 47, 60.