生技注解 英翻中 需要通順 不要用翻譯軟體翻 拜託幫幫忙!
Identification of signaling pathways of IGF-I mediated COX-2 expression in pancreatic cancer cells. (a) Western blot analysis for COX-2. Cells were pretreated with signaling inhibitors to MAPK/Erk-1/2 (UO126), or PI-3K/Akt (wortmannin, WT), as described in Section 2. Cells were subsequently stimulated for 4 h by adding rhIGF-I. IGF-I treatment resulted in a 5-fold increase in COX-2 protein expression, which was selectively mediated by the MAPK (Erk-1/2) signaling pathway. Inhibition of PI-3K/Akt signaling did not reduce COX-2 expression.
(b) COX-2 expression was investigated following treatment with inhibitors to PI-3K (LY), P38 (SB) and SAPK (SP). IGF-I mediated COX-2 induction was not blunted by pretreatment with these inhibitors prior to IGF-I exposure.
(c) Northern blot analysis for COX-2 mRNA expression. Cells were pretreated with inhibitors as described above, except that cells were treated for 1 h with rhIGF-I. Stimulation with rhIGF-I increased COX-2 mRNA in control cells, whereas this response was blunted after inhibition of MAPK/Erk-1/2 by UO126. In addition, constitutive COX-2 mRNA expression was lowered by 70% upon treatment with UO126. In contrast, inhibition of PI-3K/Akt by LY did not reduce constitutive or inducible COX-2 mRNA expression.
(d) Effect of HIF-1a inhibition on COX-2 expression. L3.6pl cells were transiently transfected with RNAi for HIF-1a. After 24 h, cells were exposed to rhIGFI. RNAi to HIF-1a markedly reduced constitutive COX-2 expression without altering the inducible response to IGF-I. b-Actin served as a loading control.
- 小君Lv 61 decade agoFavorite Answer
鑑定信號轉導途徑中IGF - I介導的COX - 2的表達在胰腺癌細胞。 （一）免疫印跡分析為環氧合酶-2 。細胞預處理信號抑製劑，以mapk/erk-1/2 （ uo126 ） ，或pi-3k/akt （ Wortmannin對，九倉） ，描述在第2條。細胞隨後刺激4 h的加入rhigf我。胰島素樣生長因子I治療，導致1 5倍增加，環氧合酶-2蛋白的表達，這是有選擇性地介導由蛋白激酶（ ERK的- 1 / 2 ）信號轉導通路。抑制pi-3k/akt信號並未減少COX - 2的表達。
（二） COX - 2的表達，考察了以下治療與抑製劑，以丕的3 K （ ly ） ， P38的（銻）和sapk （ SP ）的。中IGF - I介導的環氧合酶-2的誘導是不會減弱預處理與這些抑製劑之前， IGF - I的接觸。
（三） Northern blot分析為COX - 2 mRNA的表達。細胞預處理抑製劑如上文所述，除了細胞治療1 h後與rhigf我。刺激rhigf我增加了環氧合酶-2 mRNA在控制細胞，而這種反應是減弱後，抑制mapk/erk-1/2由uo126 。此外，本構環氧合酶-2 mRNA的表達，降低了70 ％後的待遇與uo126 。對比之下，抑制pi-3k/akt由ly並未減少構或誘導COX - 2 mRNA的表達。
（四）效果的HIF - 1的抑制COX - 2的表達。 l3.6pl細胞瞬時轉染的RNAi為中HIF - 1 。 24 h後，細胞暴露於rhigfi 。 RNAi技術，以中HIF - 1顯著減少構COX - 2的表達，而不改變誘導的反應中IGF - I 。的B -肌動充當加載控制。