Table 2. Downstream targets up-regulated by oncogenic KRAS with proteomic analysis.

				Signal Intensity			Signal Ratio
Protein	Accession	Map	P value	MOCK	G12	V12	V12/G12	V12/MOCK
S100A2	NM_005978	1q21.33	0.0001214	0.400	1.005	1.665	1.657	4.163
VIME	NM_003380	10p13	0.00000091	0.368	0.754	1.424	1.889	3.870
EEF2	NM_001961	19p13.3	0.00000313	0.454	0.922	1.515	1.643	3.337
GC	NM_000583	4q12-q13	0.001	0.480	0.934	1.582	1.694	3.296
CTSL1	NM_001912	9q21.33	0.0003414	0.635	0.708	1.708	2.412	2.690
VCP	NM_007126	9p13.3	0.002	0.599	1.010	1.551	1.536	2.589
ENOA	NM_001428	1p36.2	0.0001339	0.641	0.936	1.560	1.667	2.434
S100A11	NM_005620	1q21	0.002	0.569	0.761	1.291	1.696	2.269
CTSL1	NM_001912	9q21.33	0.001	0.730	0.802	1.551	1.934	2.125

Accession, gene bank accession number; Map, chromosome locus; MOCK, mock-transduced NHBE-T; G12, wild-type KRAS-transduced NHEB-T; V12, oncogenic mutant KRAS-transduced NHBE-T.

Proteins whose signal intensities were more than 2-fold higher in KRAS/V12 cells than in mock- and/or KRAS/G12 cells are extracted from our date of a comprehensive proteomic analysis previously described [8]. The proteins sorted are listed in this table.