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. Author manuscript; available in PMC: 2014 Mar 3.
Published in final edited form as: Annu Rev Nutr. 2013 Mar 22;33:249–269. doi: 10.1146/annurev-nutr-071812-161139

Figure 3.

Figure 3

Nutrient and hormonal regulation of sterol regulatory element–binding protein-1c (SREBP-1c) nuclear abundance. The diagram illustrates the levels of control of SREBP-1c, from gene transcription to degradation of the protein. See text for details on sites of control and regulation of SREBP-1c nuclear abundance. Insulin and liver X receptor (LXR) agonist induce (+) SREBP-1c nuclear abundance, whereas unsaturated fatty acids (UFAs), docosahexaenoic acid (DHA), and cholesterol lower (−) SREBP-1c nuclear abundance. Several enzymes are involved in covalently modifying nuclear SREBP-1, including protein kinase A (PKA), glycogen synthase kinase-3β, extracellular receptor kinase-1 or -2 (Erk1/2), or ubiquitin ligase (SCFFbw7). Several proteins are also involved in controlling SREBP processing, including insulin-inducible gene (Insig-1 or Insig-2), SREBP coactivating protein (SCAP), site-1 protease (S1P), and site-2 protease (S2P). Abbreviations: GSK-3β, glycogen synthase kinase-3β; mTORC, mammalian target of rapamycin complex; Ubxd8, ubiquitin regulatory X d8; +, induction; -, repression or inhibition; ?, mechanism not defined.