Table 1.

Regulatory mechanisms of oncogenic kinases activity by alternative splicing.

	Kinase name	Kinase type	Splicing	Regulation type
	Fyn	Cytosolic tyrosine kinase	Alternative use of exon 7a or 7b upstream of the kinase domain	Kinase activity modulation by interfering with autoinhibition
	Fak	Focal adhesion tyrosine kinase	Multiple alternative splicing upstream of the kinase domain	Kinase activity modulation by interfering with autophosphorylation
	B-Raf	Cytosolic serine/threonine kinase	Alternatively spliced exon 8b and 9b upstream of the kinase domain	Kinase activity modulation by interfering with phosphorylation and autoinhibition
Intact kinase domain	Ret	Membrane-bound tyrosine kinase receptor	C-terminal alternative splicing generating three isoforms	Modulation of signaling partners binding
	ErbB4	Membrane-bound tyrosine kinase receptor	N- and C-terminal alternative splicing generating four isoforms	Modulation of partners binding, cleavage, and subcellular localization
	FGFR1 FGFR2 FGFR3	Membrane-bound tyrosine kinase receptors	Alternative use of exon 8 or 9 generating distinct extracellular immunoglobulin-like domain III	Modified FGF binding specificity
	A-Raf	Cytosolic serine/threonine kinase	Intronic sequences retention introducing stop codons	Dominant negative
Kinase domain truncation	TrkB TrkC	Membrane-bound tyrosine kinase receptors	C-terminal alternative splicing replacing kinase domain by short amino acid sequences	Ligand sequestering, dominant negative and/or specific signaling functions
	VEGFR1 VEGFR2	Membrane-bound tyrosine kinase receptors	C-terminal alternative splicing eliminating the kinase and transmembrane domains	Synthesis of secreted/soluble extracellular ligand-binding domains