• 한국식품영양과학회지
• /
• 제45권6호
• /
• pp.835-842
• /
• 2016

PI3K/Akt 신호계는 세포 생존의 조절에 필수적인 경로로 대부분 암세포에서 활성이 증대되어 있다. 본 연구에서는 동충하초의 주요 생리활성 물질인 cordycepin에 의한 AGS 인체 위암 세포의 apoptosis 유도에 미치는 PI3K/Akt 신호계의 역할을 조사하였다. 본 연구의 결과에 의하면 cordycepin의 처리 농도의 증가에 따라 AGS 세포의 생존율은 억제되었으며, 이는 apoptosis 유도와 밀접한 관계가 있음을 핵의 형태적 변화와 flow cytometry 분석을 통하여 확인 하였다. 이러한 cordycepin의 apoptosis 유도 효과는 PI3K/Akt 신호계의 활성 저하와 연관성이 있었으며, 세포독성을 나타내지 않는 범위의 PI3K/Akt 신호계 저해제인 LY294002를 cordycepin과 동시 처리하였을 경우, cordycepin에 의한 apoptosis 유발을 더욱 증대시켰다. 그리고 cordycepin에 대한 LY294002의 apoptosis 유발 증대는 caspases (caspase-3, -8 및 -9)의 활성 증가와 poly(ADP-ribose) polymerase 단백질의 분해 증가를 촉진했다. 또한 cordycepin이 처리된 AGS 세포에서 LY294002는 apoptosis 유도에 관여하는 Bax의 발현을 증가시켰고 apoptosis 억제에 관여하는 Bcl-2의 발현은 감소시켰으며, 이는 미토콘드리아 기능 손상과 미토콘드리아에서 세포질로의 cytochrome c 유리를 증대시켰다. 따라서 PI3K/Akt 신호계의 활성 차단은 cordycepin의 항암 활성을 더욱 상승시켰으며, 이는 미토콘드리아 기능 손상과 caspase의 활성 증대를 통하여 이루어짐을 알 수 있었다.

• 한국정보통신학회:학술대회논문집
• /
• 한국해양정보통신학회 2007년도 춘계종합학술대회
• /
• pp.713-716
• /
• 2007

In this paper, we consider one of robust control system, fuzzy PI+fuzzy D controller dealing with noise, load, changed parameters of plant. We apply PI+D controller with a design for output of differential function and, we plan fuzzy controller with input for PID parameter of PI+D controller so We design control system meet with the change of environment with robust in relation to change of parameter. Fuzzy control is possessed of easy 4 rules and membership function and We design fuzzy PI+fuzzy D controller. Plant of this paper make a choice of 3 phase induction motor.

• Current Research on Agriculture and Life Sciences
• /
• 제4권
• /
• pp.7-11
• /
• 1986

한국(韓國) 지방(地方) 재래종(在來種) 고추 9계통(系統)과 미국(美國) 식물(植物) 도입국계통(導入局系統)(PI) 34개(個) 계통(系統)을 공시(公試)하여 흑색(黑色) 병징(病徵)의 탄저병(炭疽病)(Colletotrichum dematium)에 대한 저항성(抵抗性)을 검정(檢定)하였다. 적열과(赤熱果)에다 침상후(針傷後) 병원균(病原菌) 현탁액(懸濁液)을 분무(噴霧)하는 방법(方法)과 점적(點滴)하는 방법(方法)으로 접종(接種)한후 침상부위(針傷部位)를 중심(中心)으로 형성(形成)된 병반(病班) 직경(直徑)을 측정(側定)하여 저항성(低抗性)을 평가(評價)한 결과(結果)는 다음과 같다. 1) PI 201232, PI 224451, PI 257044, PI 257119, PI 257099, PI 224433, PI 244668, PI 257102, PI 173877, 남지 청룡 서동 등(等)은 발병(發病)이 가장 적어 저항성(抵抗性)으로 사료(思料)된다. 2) PI 241670, PI 244670, PI 224423 등(等)은 발병(發病)이 가장 커 이병성(罹病性)으로 사료(思料)된다. 3) 기외(其外)는 중간(中間) 정도(程度)였다.

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2003년도 추계학술대회
• /
• pp.144-144
• /
• 2003

Phosphatidylinositol 3-kinase (PI3K) and Rac play important roles that regulate cellular functions including cell survival and .migration. In the present study, we investigated the functional roles of PI3K and Rac1 pathways in H-ras-induced invasive phenotype and motility of MCF10A cells.(omitted)

• Asian Pacific Journal of Cancer Prevention
• /
• 제15권23호
• /
• pp.10463-10468
• /
• 2015

Opisthorchis viverrini (Ov) infection is the major etiological factor for cholangiocarcinoma (CCA), especially in northeast Thailand. We have previously reported significant involvement of PI3K/AKT/PTEN and $Wnt/{\beta}$-catenin in human CCA tissues. The present study, therefore, examined the expression and activation of PI3K/AKT/PTEN and $Wnt/{\beta}$-catenin signaling components during Ov-induced cholangiocarcinogenesis in a hamster animal model. Hamsters were divided into two groups; non-treated and Ov plus NDMA treated. The results of immunohistochemical staining showed an upregulation of PI3K/AKT signaling as determined by elevated expression of the $p85{\alpha}$-regulatory and $p110{\alpha}$-catalytic subunits of PI3K as well as increased expression and activation of AKT during cholangiocarcinogenesis. Interestingly, the staining intensity of activated AKT (p-AKT) increased in the apical regions of the bile ducts and strong staining was detected where the liver fluke resides. Moreover, PTEN, a negative regulator of PI3K/AKT, was suppressed by decreased expression and increased phosphorylation during cholangiocarcinogenesis. We also detected upregulation of $Wnt/{\beta}$-catenin signaling as determined by increased positive staining of Wnt3, Wnt3a, Wnt5a, Wnt7b and ${\beta}$-catenin, corresponded with the period of cholangiocarcinogenesis. Furthermore, nuclear staining of ${\beta}$-catenin was observed in CCA tissues. Our results suggest the liver fluke infection causes chronic inflammatory conditions which lead to upregulation of the PI3K/AKT and $Wnt/{\beta}$-catenin signaling pathways which may drive CCA carcinogenesis. These results provide useful information for drug development, prevention and treatment of CCA.

• Kyungpook Mathematical Journal
• /
• 제51권3호
• /
• pp.311-322
• /
• 2011

In this paper, we generalize the definition of a closure operator for a finite matroid to a pi-space and obtain the corresponding closure axioms. Then we discuss some properties of pi-spaces using the closure axioms and prove the non-existence for the dual of a pi-space. We also present some results on the automorphism group of a pi-space.

• 대한수학회지
• /
• 제32권3호
• /
• pp.371-387
• /
• 1995

Let X be a compact polyhedron, H a normal subgroup of the fundamental group $\pi_1(X)$ of X and $f : X \longrightarrow X$ a selfmap such that $f_piH \subset H$, where f_\pi : \pi_1(X) \longrightarrow \pi_1(X)$ is the induced homomorphism by f.

• Molecules and Cells
• /
• 제38권6호
• /
• pp.535-539
• /
• 2015

Olfactory stimulation activates multiple signaling cascades in order to mediate activity-driven changes in gene expression that promote neuronal survival. To date, the mechanisms involved in activity-dependent olfactory neuronal survival have yet to be fully elucidated. In the current study, we observed that olfactory sensory stimulation, which caused neuronal activation, promoted activation of the phosphatidylinositol 3'-kinase (PI3K)/Akt pathway and the expression of Bcl-2, which were responsible for olfactory receptor neuron (ORN) survival. We demonstrated that Bcl-2 expression increased after odorant stimulation both in vivo and in vitro. We also showed that odorant stimulation activated Akt, and that Akt activation was completely blocked by incubation with both a PI3K inhibitor (LY294002) and Akt1 small interfering RNA. Moreover, blocking the PI3K/Akt pathway diminished the odorantinduced Bcl-2 expression, as well as the effects on odorant-induced ORN survival. A temporal difference was noted between the activation of Akt1 and the expression of Bcl-2 following odorant stimulation. Blocking the PI3K/Akt pathway did not affect ORN survival in the time range prior to the increase in Bcl-2 expression, implying that these two events, activation of the PI3K pathway and Bcl-2 induction, were tightly connected to promote post-translational ORN survival. Collectively, our results indicated that olfactory activity activated PI3K/Akt, induced Bcl-2, and promoted long term ORN survival as a result.

• BMB Reports
• /
• 제46권2호
• /
• pp.103-106
• /
• 2013

Phosphoinositide 3-kinases (PI3Ks) play key roles in synaptic plasticity and cognitive functions in the brain. We recently found that genetic deletion of $PI3K{\gamma}$, the only known member of class IB PI3Ks, results in impaired N-methyl-D-aspartate receptor-dependent long-term depression (NMDAR-LTD) in the hippocampus. The activity of RalA, a small GTP-binding protein, increases following NMDAR-LTD inducing stimuli, and this increase in RalA activity is essential for inducing NMDAR-LTD. We found that RalA activity increased significantly in $PI3K{\gamma}$ knockout mice. Furthermore, NMDAR-LTD-inducing stimuli did not increase RalA activity in $PI3K{\gamma}$ knockout mice. These results suggest that constitutively increased RalA activity occludes further increases in RalA activity during induction of LTD, causing impaired NMDAR-LTD. We propose that $PI3K{\gamma}$ regulates the activity of RalA, which is one of the molecular mechanisms inducing NMDAR-dependent LTD.

• The Korean Journal of Physiology and Pharmacology
• /
• 제24권5호
• /
• pp.423-431
• /
• 2020

This study aimed to evaluate the effect of curcumin on brain hypoxic-ischemic (HI) damage in neonatal rats and whether the phosphoinositide 3-kinase (PI3K)/Akt/vascular endothelial growth factor (VEGF) signaling pathway is involved. Brain HI damage models were established in neonatal rats, which received the following treatments: curcumin by intraperitoneal injection before injury, insulin-like growth factor 1 (IGF-1) by subcutaneous injection after injury, and VEGF by intracerebroventricular injection after injury. This was followed by neurological evaluation, hemodynamic measurements, histopathological assessment, TUNEL assay, flow cytometry, and western blotting to assess the expression of p-PI3K, PI3K, p-Akt, Akt, and VEGF. Compared with rats that underwent sham operation, rats with brain HI damage showed remarkably increased neurological deficits, reduced right blood flow volume, elevated blood viscosity and haematocrit, and aggravated cell damage and apoptosis; these injuries were significantly improved by curcumin pretreatment. Meanwhile, brain HI damage induced the overexpression of p-PI3K, p-Akt, and VEGF, while curcumin pretreatment inhibited the expression of these proteins. In addition, IGF-1 treatment rescued the curcumin-induced down-regulated expression of p-PI3K, p-Akt, and VEGF, and VEGF overexpression counteracted the inhibitory effect of curcumin on brain HI damage. Overall, pretreatment with curcumin protected against brain HI damage by targeting VEGF via the PI3K/Akt signaling pathway in neonatal rats.