Table 1.

List of RTKs whose functions are affected by intracellular localizations.

Name of RTK	Description	Refs.
FLT3-ITD	In ER, FLT3-ITD activates STAT5, while in membrane FLT3-ITD strongly activates MAPK and PI3K	[16,17]
FLT3-ITD, FLT3-TKD, FLT3-N676K	After the addition of tyrosine kinase inhibitor (TKI) AC220, a intracellular localization of FLT3-ITD, as well as FLT3-TKD was changed to plasma membrane, which is similar to FLT3-WT or FLT3-N676K, another type of FLT3 TKD	[18]
FLT3-TKD	NPM1c alters the cellular localization of FLT3-TKD from the cell surface to ER, which may lead to the aberrant activation of STAT5.	[19]
FLT3-ITD	In plasma membrane, FLT3ITD activates AKT signaling pathway and produces of p22phox-generated H2O2	[20]
PDGFR	The precursor of PDGF receptor is converted to a 180-kD mature form. Intracellular activation of PDGFR by the v-Sis protein has been related to sis-mediated transformation.	[41,42]
KIT mutation	KIT mutations induce intracellular retention and activation of an immature form of the KIT protein in gastrointestinal stromal tumors	[43], [44], [45], [46]
CSF1 mutation	CSF1 activating mutation retarded in transport to the cell surface and were phosphorylated on tyrosine in the absence of ligand, resulting in CSF-1-independent signals for cell growth and transformation.	[47]
FGFR3 mutation	The highly activated tyrosine phosphorylated SADDAN mutants accumulates its immature and phosphorylated from in the ER, which fails to be degraded. ER retained constitutively active FGFR3 activates JAK/STAT pathway.	[48]
ALK mutation	Constitutive active form of ALK impairs receptor trafficking. Mutated ALK variants were essentially intracellular and were largely retained in the reticulum/Golgi compartments, and this is corroborated with a defect of N-linked glycosylation	[49]
ROS1 RTK fusion proteins	SDC4-ROS1 and SLC34A2-ROS1 fusion oncoproteins resided on endosomes and activated the MAPK pathway.	[50]