Galien R, Emanoil-Ravier R, Mercier G
Laboratoire des Rétrovirus et Rétrotransposons des Vertébrés, UPR 0043 CNRS, Hopital Saint-Louis, Paris, France.
Oncogene. 1994 Apr;9(4):1101-8.
We have previously shown that a Long Terminal Repeat (LTR) of the Intracisternal A-type Particle (IAP) element was activated by ras oncogenes. Here we show that, like the somatostatin CRE (som CRE) and the collagenase TPA Response Element (coll TRE), the IAP CRE is activated by c-jun and that Val 12 Ha-ras cooperates with c-jun to activate these motifs. Neither jun-B nor jun-D activated the IAP CRE, although they were able to act on the som CRE and the coll TRE and to synergize with ras. The CREB factor activated both CREs and modestly inhibited the coll TRE, but diminished the effect of ras on the coll TRE. Finally, forskolin was shown to cooperate with Ha-ras to activate the CRE and the coll TRE. Taken together, these results show that CREB is not involved in ras activation of the CRE and suggest that c-jun is at least one of the elements implicated in this phenomenon.
我们之前已经表明，颅内A 型颗粒（IAP）元件的长末端重复序列（LTR）被ras癌基因激活。在此我们表明，与生长抑素CRE（som CRE）和胶原酶TPA反应元件（coll TRE）一样，IAP CRE被c-jun激活，并且Val 12 Ha-ras与c-jun协同激活这些基序。尽管Jun-B和Jun-D能够作用于som CRE和coll TRE并与ras协同作用，但它们均未激活IAP CRE。CREB因子激活了这两种CRE，并适度抑制了coll TRE，但减弱了ras对coll TRE的作用。最后，已证明福斯可林与Ha-ras协同激活CRE和coll TRE。综上所述，这些结果表明CREB不参与ras对CRE的激活，并提示c-jun至少是参与此现象的元件之一。
