Table 1.

Inj	SmβInt	SmILK		SmPINCH		SmNck2		SmVKR1			GVBD	GVBD + L-Arg
		wt	del	wt	del	wt	del	wt	ca	dk	%	%
1		+									0
2				+							0
3	+										0
4								+			0	90
5									+		90
6										+		0
7	+	+		+							0
8		+		+				+			0	90
9	+			+				+			0	100
10	+	+						+			0	90
11	+	+		+				+			80	90
12	+		+	+				+			0	50
13	+	+*QLT		+		+		+			0
14	+	+			+			+			0	90
15	+	+		+			+	+			10
16	+	+		+					+		100
17	+	+		+						+	0
18	+	+		+				SmVKR2			0
19	+	+		+				SER			0
20	+	+		+				SmIR1			0
21	+	+		+				SmIR2			0

Summarized are 21 transfection experiments in Xenopus oocytes and germinal vesicle breakdown (GVBD, in %) as physiological assay with different constructs alone or in combination (indicated by single or multiple “+”-signs). Inj, injection experiment number; SmβInt = Smβ-Int1; wt, wildtype; del, deletion mutant (SmILK: SmILKΔAnk1; SmPINCH: SmPINCHΔLIM4; SmNck2: SmNck2ΔSH3; SmVKR1 dk, dead kinase [22]). Injections 18–21, control experiments in which SmVKR1 was replaced by SmVKR2 [22], SER (S. mansoni EGF Receptor; [45, 46]), or the insulin receptor orthologs SmIR 1 and SmIR2 [47]. In these cases no GVBD was induced (compare to Inj 11). ca, constitutively active (SmVKR1, SmVKR1^YYRE [22]); GVBD values (%) were determined as previously described and represent the mean of two independent experiments with 10 oocytes each [15, 45];

*QLT, inhibitor of the integrin-linked kinase (1 μM); L-Arg, L-Arginine; empty boxes in the last two columns: not determined.