. 1998 Mar;9(3):561–573. doi: 10.1091/mbc.9.3.561

Table 1.

Hyperosmotic glucose, HGF, and TNFα stimulate JNK1 activity, which is blocked by expression of dominant-negative Ras^N17, dominant-negative Rac1^N17, dominant-negative Cdc42^N17, dominant-negative SEK1, and dominant-negative JNK1, but not by expression of dominant-negative c-Jun(TAM67)

Glucose	null	Ras^N17	Rac1^N17	Cdc42^N17	SEK1⁻	JNK1⁻	c-Jun(TAM67)
Control	3,719 ± 570	1,627 ± 180^a	833 ± 180^a	533 ± 90^a	1,605 ± 220^a	2,172 ± 300^a	4,438 ± 190
Glucose	10,168 ± 2,400^b	1,377 ± 330^a	929 ± 50^a	1,184 ± 320^a	2,567 ± 140^a	2,107 ± 110^a	11,313 ± 1,050^b
HGF	12,585 ± 1,820^b	1,711 ± 410^a	1,263 ± 290^a	1,517 ± 280^a	2,564 ± 380^a	1,873 ± 220^a	11,647 ± 1,670^b
TNFα	12,440 ± 1,750^b	1,710 ± 240^a	1,596 ± 300^a	1,851 ± 60^a	1,897 ± 180^a	2,559 ± 145^a	12,647 ± 770^b

Hepatocytes were infected with either control plasmid poly-l-lysine adenovirus or dominant-negative Ras N17/Rac1 N17/Cdc42 N17/SEK1⁻/JNK1⁻ poly-l-lysine adenovirus (250 moi), followed by culture as described in MATERIALS AND METHODS. In a parallel experiment, hepatocytes were infected with a recombinant adenovirus (250 moi) to express a nontransactivatable dominant-negative c-Jun(TAM67). After 24 h to allow expression of dominant-negative gene products, hepatocytes were treated for 10 min with either media control, 50 mM glucose, 1 ng/μl HGF, or 1 ng/μl TNFα. After 10 min, media were aspirated and cells frozen. Hepatocytes were lysed and subjected to immunoprecipitation followed by immune complex kinase assays for JNK1. Activities shown are expressed as cpm incorporated into substrate versus media control treatment (5000 cpm/pmol) and are the means ± SE from two to five experiments, each performed in duplicate.

p < 0.05 decrease compared with corresponding value in null/control plasmid infected.

p < 0.05 increase compared with control.