새 아침 평신도의 기도(302)
사순절 고난을 묵상하면서 보낸지가
엊그제 같은데 벌써 부활 4주차를 맞았습니다.
십자가의 삶은 간 곳 없고, 오히려 화려한
꽃처럼 축복만을 달라고 할 때가 많습니다.
지난주 독서강독을 통해 읽은 행동하는 신앙인
‘본 훼퍼’의 글 내용을 인용합니다.
“회개란 단순히 잘못했다고 눈물을 흘리는 것이 아니다.
회개란 그 삶이 달라지는 것이다”
그러니까 삶의 방향이 달라지고, 추구하는 가치관이
부족한 것이 없는 일상일지라도, 오늘은 이 말씀을
묵상하며 출발하기를 기도하는 아침입니다.
“이 백성이 입술로는 나를 공경하여도, 마음은
나에게서 멀리 떠나 있구나” (마르코 7:6)
대한성공회 서울교구 평신도국 최호용 드림
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Raptor and Rictor, respectively. To investigate the roles of mTORC1 and mTORC2 in this pathway, the requirement for Raptor or Rictor in the antiapoptotic function of Notch was assessed. Cellular pools of Rictor (mTORC2) or Raptor (mTORC1) Oakley Sunglasses Outlet
were independently depleted using siRNA (Figure 4c). Depletion of Rictor abrogated NIC GFP function (Figure 4b), whereas reducing the levels of Raptor or the scrambled siRNA (included as a control in all experiments) had no effect on NIC mediated inhibition of death (Figure 4b). Although the functional interaction between mTORC2 and Notch signaling revealed by these experiments was consistent with the demonstrated requirement for Akt and its phosphorylation on S473, the requirement for mTORC2 for Notch mediated phosphorylation of Akt remained to be established. This was again monitored in conditions where the cellular levels of mTOR, Rictor, or Raptor were reduced by siRNA. Depletion of mTOR or Rictor inhibited the phosphorylation of Akt on S473 in NIC expressing cells (Figure 4d and f), whereas the depletion of Raptor was without effect (Figure 4e). As mTOR and Rictor dependence of a signaling cascade is consistent with the activation of Akt on S473,19 site directed mutants were employed to test whether AktS473 was a functional effector of the NIC signaling cascade in the regulation of cell survival.