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. Author manuscript; available in PMC: 2014 Jun 16.
Published in final edited form as: Curr Biol. 2012 May 22;22(10):R414–R424. doi: 10.1016/j.cub.2012.03.004

Figure 2. Kes1 integrates PtdIns-4-P signaling, sterols, TGN trafficking control, and larger cellular physiological responses.

Figure 2

Kes1 is recruited to Golgi membranes by virtue of its ability to bind PtdIns-4-P where it clamps availability of this phosphoinositide and functions as a trafficking ‘brake’ [62]. Sterol binding at the TGN releases Kes1 from the membrane, thereby releasing the trafficking brake. Larger consequences of this negative regulation of membrane trafficking include TGN/endosomal sphingolipid metabolism-mediated control of cell proliferation, TOR signaling, and execution of nitrogen stress transcriptional responses.