. Author manuscript; available in PMC: 2017 Dec 1.

Published in final edited form as: Biochim Biophys Acta. 2016 Sep 15;1866(2):189–196. doi: 10.1016/j.bbcan.2016.09.003

Table 1.

Phosphorylation sites on TIF-IA

Phosphorylation Sites	Flanking Seq	Consensus	Kinase/ Phosphatase	Function	Interaction with Pol I or SL-1	Stress	Reference
Ser44	FNSPPRKTV	[S/T]PX[K/R]	CDK	activate	no change		[52]
Ser44	FNSPPRKTV	[S/T]PX[K/R]	PP2A	inactivate	no change	Rapamycin	[52]
Ser170/172	DVSDSDDED	SxxE/D	CK2	activate	disrupts RNA Pol I interaction	AKT as upstream event	[53]
Ser170/172	DVSDSDDED	SxxE/D	FCP1	activate	enhance RNA Pol I interaction		[53]
Ser199	IARYVPSTP	unknown	unknown	inactivate	disrupts RNA Pol I and TIF-IB/SL-1 interaction	Rapamycin	[28]
Thr200	VPSTP	VPxTP	JNK	inactivate	disrupts RNA Pol I and TIF-IB/SL-1 interaction		[52]
Ser633	FDTHF- RSPSSSVGSPPVLYMQP- SPL		ERK	activate		serum stimulation	[54].
Ser635	DTHFRSPSSSVGSPPVLY	LRRVxSxxNL	AMPK	inactivate	disrupt SL-1 interaction	glucose free	[56]
		MKKSxSxxDV				AICAR	[57]
		IxHRxSxxEI
Ser649	FDTHF- RSPSSSVGSPPVLYMQP- SPL	R/LxRxxS/T	RSK	activate	phosphorylation of S649 by RSK is a pre-requisite for S633 by ERK	serum stimulation	[56]