• Journal of Microbiology and Biotechnology
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• 제24권2호
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• pp.287-294
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• 2014

The transcription factor E2F1 is active during G1 to S transition and is involved in the cell cycle and progression. A recent study reported that increased E2F1 is associated with DNA damage and tumor development in several tissues using transgenic models. Here, we show that E2F1 expression is regulated by tristetraprolin (TTP) in prostate cancer. Overexpression of TTP decreased the stability of E2F1 mRNA and the expression level of E2F1. In contrast, inhibition of TTP using siRNA increased the E2F1 expression. E2F1 mRNA contains three AREs within the 3'UTR, and TTP destabilized a luciferase mRNA that contained the E2F1 mRNA 3'UTR. Analyses of point mutants of the E2F1 mRNA 3'UTR demonstrated that ARE2 was mostly responsible for the TTP-mediated destabilization of E2F1 mRNA. RNA EMSA revealed that TTP binds directly to the E2F1 mRNA 3'UTR of ARE2. Moreover, treatment with siRNA against TTP increased the proliferation of PC3 human prostate cancer cells. Taken together, these results demonstrate that E2F1 mRNA is a physiological target of TTP and suggests that TTP controls proliferation as well as migration and invasion through the regulation of E2F1 mRNA stability.

• Molecules and Cells
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• 제21권3호
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• pp.356-359
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• 2006

The transcription factor E2F1 coordinates cell cycle progression and induces apoptosis in response to DNA damage stress. Aside from DNA damage, the role of E2F1 in the endoplasmic reticulum (ER) stress signaling pathways is unclear. We found that $E2F1^{-/-}$ murine embryonic fibroblasts (MEFs) are resistant to apoptosis triggered by the ER stress inducer thapsigargin. In addition, E2F1 deficiency results in enhanced phosphorylation of eukaryotic translation initiation factor $2{\alpha}$ ($elF2{\alpha}$). These results therefore indicate that E2F1 deficiency increases phosphorylation of $elF2{\alpha}$ in response to ER stress triggered by thapsigargin, and suggest that the reduction in ER stress-induced apoptosis in E2F1-deficient cells is related to the high level of $elF2{\alpha}$ phosphorylation.

• BMB Reports
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• 제42권10호
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• pp.691-696
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• 2009

The E2F gene family appears to regulate the proliferation and differentiation of events that are required for adipogenesis. Pref-1 is a transmembrane protein that inhibits adipocyte differentiation in 3T3-L1 cells. In this study, we found that the expression of pref-1 is regulated by the transcription factor E2F1. The expression of pref-1 and E2F1 was strongly induced in preadipocytes and at the late differentiation stage. Using luciferase reporter assay, ChIP assay and EMSA, we found that the -211/-194 region of the pref-1 promoter is essential for the binding of E2F1 as well as E2F1-dependent transcriptional activation. Knockdown of E2F1 reduced both pref-1 promoter activity and the level of pref-1 mRNA. Taken together, our data suggest that transcriptional activation of pref-1 is stimulated by E2F1 protein in adipocytes.

• 대한수학회논문집
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• 제20권4호
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• pp.645-648
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• 2005

Let K be a Galois extension of a field F with G = Gal(K/F). Let L be an extension of F such that $K\;{\otimes}_F\;L\;=\; N_1\;{\oplus}N_2\;{\oplus}{\cdots}{\oplus}N_k$ with corresponding primitive idempotents $e_1,\;e_2,{\cdots},e_k$, where Ni's are fields. Then G acts on $\{e_1,\;e_2,{\cdots},e_k\}$ transitively and $Gal(N_1/K)\;{\cong}\;\{\sigma\;{\in}\;G\;/\;{\sigma}(e_1)\;=\;e_1\}$. And, let R be a commutative F-algebra, and let P be a prime ideal of R. Let T = $K\;{\otimes}_F\;R$, and suppose there are only finitely many prime ideals $Q_1,\;Q_2,{\cdots},Q_k$ of T with $Q_i\;{\cap}\;R\;=\;P$. Then G acts transitively on $\{Q_1,\;Q_2,{\cdots},Q_k\},\;and\;Gal(qf(T/Q_1)/qf(R/P))\;{\cong}\;\{\sigma{\in}\;G/\;{\sigma}-(Q_1)\;=\;Q_1\}$ where qf($T/Q_1$) is the quotient field of $T/Q_1$.

• Journal of the Korean Society for Industrial and Applied Mathematics
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• 제11권2호
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• pp.9-14
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• 2007

A signed 3-partite graph is a 3-partite graph in which each edge is assigned a positive or a negative sign. Let G(U, V, W) be a signed 3-partite graph with $U\;=\;\{u_1,\;u_2,\;{\cdots},\;u_p\},\;V\;=\;\{v_1,\;v_2,\;{\cdots},\;v_q\}\;and\;W\;=\;\{w_1,\;w_2,\;{\cdots},\;w_r\}$. Then, signed degree of $u_i(v_j\;and\;w_k)$ is $sdeg(u_i)\;=\;d_i\;=\;d^+_i\;-\;d^-_i,\;1\;{\leq}\;i\;{\leq}\;p\;(sdeg(v_j)\;=\;e_j\;=\;e^+_j\;-\;e^-_j,\;1\;{\leq}\;j\;{\leq}q$ and $sdeg(w_k)\;=\;f_k\;=\;f^+_k\;-\;f^-_k,\;1\;{\leq}\;k\;{\leq}\;r)$ where $d^+_i(e^+_j\;and\;f^+_k)$ is the number of positive edges incident with $u_i(v_j\;and\;w_k)$ and $d^-_i(e^-_j\;and\;f^-_k)$ is the number of negative edges incident with $u_i(v_j\;and\;w_k)$. The sequences ${\alpha}\;=\;[d_1,\;d_2,\;{\cdots},\;d_p],\;{\beta}\;=\;[e_1,\;e_2,\;{\cdots},\;e_q]$ and ${\gamma}\;=\;[f_1,\;f_2,\;{\cdots},\;f_r]$ are called the signed degree sequences of G(U, V, W). In this paper, we characterize the signed degree sequences of signed 3-partite graphs.

• 한국정보통신학회논문지
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• 제9권2호
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• pp.380-389
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• 2005

부동소수점 나눗셈에서 많이 사용하는 골드스미트 나눗셈 알고리즘은 일정한 횟수의 곱셈을 반복한다. 본 논문에서는 오차가 정해진 값보다 작아질 때까지 곱셈을 반복하여 나눗셈을 수행하는 가변 시간 골드스미트 부동소수점 나눗셈 알고리즘을 제안한다. 부동소수점 나눗셈 ‘$\frac{N}{F}$'는 'T=$\frac{1}{F}+e_t$'를 분모와 분자에 곱하면 ’$\frac{TN}{TF}=\frac{N_0}{F_0}$'가 된다. ’$R_i=(2-e_r-F_i),\;N_{i+1}=N_i{\ast}R_i,\;F_{i+1}=F_i{\ast}R_i$, i$\in${0,1,...n-1}'를 반복한다. 중간 곱셈 결과는 소수점이하 p 비트 미만을 절삭하며, 절삭 오차는 ‘$e_r=2^{-p}$', 보다 작다. p는 단정도실수에서 29, 배정도실수에서 59이다. ’$F_i=1+e_i$'이라고 하면 ‘$F_{i+1}=1-e_{i+1},\;e_{i+1},\;e_{i+1}'이 된다. '$[F_i-1]<2^{\frac{-p+3}{2}}$'이면, ’$e_{i+1}<16e_r$'이 부동소수점으로 표현 가능한 최소값보다 작아지며, ‘$N_{i+1}\risingdotseq\frac{N}{F}$이다. 본 논문에서 제안한 알고리즘은 입력 값에 따라서 곱셈 횟수가 다르므로, 평균 곱셈 횟수를 계산하는 방식을 도출하고, 여러 크기의 근사 역수 테이블($T=\frac{1}{F}+e_t$)에서 단정도실수 및 배정도실수의 나눗셈 계산에 필요한 평균 곱셈 횟수를 계산한다. 이들 평균 곱셈 횟수를 종래 알고리즘과 비교하여 본 논문에서 제안한 알고리즘의 우수성을 증명한다. 본 논문에서 제안한 알고리즘은 오차가 일정한 값보다 작아질 때까지만 반복 연산을 수행하므로 나눗셈기의 성능을 높일 수 있다. 또한 최적의 근사 역수 테이블을 구성할 수 있다. 본 논문의 연구 결과는 디지털 신호처리, 컴퓨터 그라픽스,, 멀티미디어, 과학 기술 연산 등 부동소수점 계산기가 사용되는 분야에서 폭 넓게 사용될 수 있다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권8호
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• pp.3817-3823
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• 2014

Background: The MDM2 oncogene, a negative regulator of p53, has a functional polymorphism in the promoter region (SNP309) that is associated with multiple kinds of cancers including non-melanoma skin cancer. SNP309 has been shown to associate with accelerated tumor formation by increasing the affinity of the transcriptional activator Sp1. It remains unknown whether there are other factors involved in the regulation of MDM2 transcription through a trans-regulatory mechanism. Methods: In this study, SNP309 was verified to be associated with overexpression of MDM2 in tumor cells. Bioinformatics predicts that the T to G substitution at SNP309 generates a stronger E2F1 binding site, which was confirmed by ChIP and luciferase assays. Results: E2F1 knockdown downregulates the expression of MDM2, which confirms that E2F1 is a functional upstream regulator. Furthermore, tumor cells with the GG genotype exhibited a higher proliferation rate than TT, correlating with cyclin D1 expression. E2F1 depletion significantly inhibits the proliferation capacity and downregulates cyclin D1 expression, especially in GG genotype skin fibroblasts. Notably, E2F1 siRNA effects could be rescued by cyclin D1 overexpression. Conclusion: Taken together, a novel modulator E2F1 was identified as regulating MDM2 expression dependent on SNP309 and further mediates cyclin D1 expression and tumor cell proliferation. E2F1 might act as an important factor for SNP309 serving as a rate-limiting event in carcinogenesis.

• 충청수학회지
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• 제23권4호
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• pp.679-689
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• 2010

By developing and using certain operators like those initiated by Burchnall-Chaundy, the authors aim at investigating several decomposition formulas associated with the $Kamp{\acute{e}}$ de $F{\acute{e}}riet$ function $F_{2:0;0}^{0:3;3}$ [x, y]. For this purpose, many operator identities involving inverse pairs of symbolic operators are constructed. By employing their decomposition formulas, they also present a new group of integral representations of Eulerian type for the $Kamp{\acute{e}}$ de $F{\acute{e}}riet$ function $F_{2:0;0}^{0:3;3}$ [x, y], some of which include several hypergeometric functions such as $_2F_1$, $_3F_2$, an Appell function $F_3$, and the $Kamp{\acute{e}}$ de $F{\acute{e}}riet$ functions $F_{2:0;0}^{0:3;3}$ and $F_{1:0;1}^{0:2;3}$.

• Kyungpook Mathematical Journal
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• 제58권4호
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• pp.747-759
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• 2018

A graph G = (V (G), E(G) of order n = |V (G)| and size m = |E(G)| is said to be odd harmonious if there exists an injection $f:V(G){\rightarrow}\{0,\;1,\;2,\;{\ldots},\;2m-1\}$ such that the induced function $f^*:E(G){\rightarrow}\{1,\;3,\;5,\;{\ldots},\;2m-1\}$ defined by $f^*(uv)=f(u)+f(v)$ is bijection. While a bipartite graph G with partite sets A and B is said to be bigraceful if there exist a pair of injective functions $f_A:A{\rightarrow}\{0,\;1,\;{\ldots},\;m-1\}$ and $f_B:B{\rightarrow}\{0,\;1,\;{\ldots},\;m-1\}$ such that the induced labeling on the edges $f_{E(G)}:E(G){\rightarrow}\{0,\;1,\;{\ldots},\;m-1\}$ defined by $f_{E(G)}(uv)=f_A(u)-f_B(v)$ (with respect to the ordered partition (A, B)), is also injective. In this paper we prove that odd harmonious graphs and bigraceful graphs are equivalent. We also prove that the number of distinct odd harmonious labeled graphs on m edges is m! and the number of distinct strongly odd harmonious labeled graphs on m edges is [m/2]![m/2]!. We prove that the Cartesian product of strongly odd harmonious trees is strongly odd harmonious. We find some new disconnected odd harmonious graphs.

• 대한가정학회지
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• 제28권4호
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• pp.1.1-13
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• 1990

Authors have performed the sensory evaluation tests according to each given items after selecting various lines in order to assess the visual effects by the lines in cloth designing. The evaluations were done by means of ranking tests followed by paired comparison tests. The results obtained were as follows : 1. In the item in than "Shoulder width looks wide", the design C3 showed the best visual effect, and then B1, F8, and A5 comes in order. In "Shoulder width looks narrow", they were A2, F5, F7, and B2 in order. 2. In "Bust looks big", the effect was best in F9, and then B1, F5, C3, and A5 and order. "Bust looks small" item showed A3, C1, and F1 in order. 3. In "Waist looks thick", they were B2, D1, and F7 while in "Waist looks thin", they were B3, F8, and D6 in order. 4. In the item in that "Hip looks big", the best effect was in F9, and then E3, C2, and B4 in order. In "Hip looks small", the best one was C1, and then comes. E1, F6, and F8. 5. In "Upper body looks thick", they were D2, D4, F8, C3 and A5 in order whild in "Upper body looks thin", they were A1, F5, and D7 in order. 6. In the item "Lower body lookds thick", they were F9, C2, E3, B3, and D3 in order. In "Lower body looks thin", the best one was C1, and then D1, E2, F6, and F8 comes in order. 7. In "whole body looks thick", they were F9, F3, D3, and A5, and in "Whole body looks thin", they were F5, A1, C1, and D6 in order. 8. In "Height looks tall", the effects were in order of A4, D6, E1, and F7 while in "Height looks short", they were E3, F9, B4, D2, and D1. 8. In "Height looks tall", the effects were in order of A4, D6, E1, and F7 while in "Height looks short", they were E3, F9, B4, D2, and D1. F9, B4, D2, and D1.