[問題] 麻煩幫忙解釋一下 paper

[ZeroTeacher (零老師)]

Paper :  THE JOURNAL OF BIOLOGICAL CHEMISTRY
         Vol. 279, No. 47, Issue of November 19, pp. 49420–49429, 2004

   Critical Role of Endogenous Akt/IAPs and MEK1/ERK Pathways in
   Counteracting Endoplasmic Reticulum Stress-induced Cell Death*

   Ping Hu侩, Zhang Han, Anthony D. Couvillon, and John H. Exton
 闺teracting Endoplasmic Reticulum Stress-induced Cell Death


我妹妹看這篇 paper ，有一段看不太懂意思，麻煩大家幫忙翻譯一下要義：

黃色部份...先謝謝各位

To elucidate whether activation of the PI3K/Akt pathway is
required to protect cells from ER stress-induced cell death, we
first assessed the effect of the PI3K inhibitor LY294002. As
shown by phase-contrast microscopy and a cell viability assay
(MTT assay) in Fig. 2 (C and D), co-incubation with LY294002
significantly sensitized MCF-7 cells to thapsigargin- or tunicamycin-
induced cell death. LY294002 treatment alone had no
effect on cell viability. Similar results were obtained when the
same experiments were performed with H1299 cells (Fig. 2D).
To further confirm that Akt signaling is protective of cell survival
during ER stress, we established MCF-7 cell pools stably
expressing HA-tagged dominant-negative (DN) Akt in which a
point mutation (K197M) was introduced at a site required for
kinase activity. Control cells were transfected with empty vector.
Stable transfectants were identified by Western blotting
with an HA-specific monoclonal antibody. A cell viability assay
showed that ectopic expression of DN-Akt significantly increased
thapsigargin- and tunicamycin-induced cell death (Fig.
2E). Similar results were obtained in H1299 cell expressing
DN-Akt (data not shown). These results provide evidence that
activation of the PI3K/Akt pathway is a critical cell survival
response to ER stress.

Akt-dependent Activation of mTOR Is Not Required for Aktmediated
Survival Signaling in ER Stress—Recent research
has shown that mTOR, an established Akt effector, is essential
for Akt-mediated survival signaling . There is also
much evidence that mitogens and growth factors stimulate
phosphorylation of mTOR at Ser2448 . It was therefore
interesting to investigate the role of mTOR in regulation of ER
stress considering its critical controlling role in protein synthesis.
Acute phosphorylation of mTOR at Ser2448 was found in
MCF-7 cells treated with thapsigargin or tunicamycin, which
was blocked by either LY249002 or expression of DN-Akt (Fig.
3A). Next, we tested whether activated mTOR contributes to
cell survival during ER stress. As shown in Fig. 3B, co-incubation
of MCF-7 cells with rapamycin, an inhibitor of mTOR, did
not increase ER stress-induced cell death. Our data indicate
that ER stress induces phosphorylation of mTOR in an Akt-dependent
manner; however, this is not involved in cell survival.

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◆ From: 211.74.178.133
推 HIbaby:在ER的stress狀態下, 需要經由akt來的傳遞生存訊息
→ HIbaby:但是mTOR雖然被林酸化, 但是並不包含在ER stress的調空中
→ HIbaby:大致上是這個意思..
→ HIbaby:抱歉, 系統很難選好字...
※ 編輯: ZeroTeacher     來自: 211.74.178.133       (11/24 21:15)
推 ZeroTeacher:謝謝你....Orz
推 HIbaby:後面你多出來的是說 mTOR同位置被磷酸化 也發現在其他報告
→ HIbaby:跟細胞增殖相關的研究中被發現, 所以探討是否也在ER stress
→ HIbaby:也有參與.. 然後家了阻礙劑啦..etc. 最後發現沒有啥關係
推 ZeroTeacher:再次感謝 ....o(〒﹏〒)o