• Archives of Pharmacal Research
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• v.25 no.3
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• pp.375-380
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• 2002

Cytochrome P4501A2 (CYP1A2) is a member of the cytochrome P450 family of isozymes involved in the phase I drug metabolism of vertebrates. CYP1A2 is responsible for the activation of a number of aromatic amines to mutagenic and carcinogenic forms. Thus, the level of CYP1A2, which varies among different populations, may determine an individual's susceptibility to these chemicals. We have previously reported on the importance of a cis element named PRB (protected region B) in the regulation of human Cytochrome P4501A2 (CYP1A2) gene, which appeared to act as a positive regulatory element. Closer examination of the PRB sequence (-2218 to -2187 bp) revealed a putative AP-1 binding site, TGACTAA, at -2212 bp (Chung and Bresnick, 1997). To elucidate the role of AP-1 in CYP1A2 regulation, we transiently overexpressed c-Jun and c-Fos transcription factors in human hepatoma HepG2 cells, and examined their influence on the CYP1A2 promoter activity by reporter gene assays. Cotransfection of the c-Jun and the c-Fos expression vectors increased the induced transactivation by five to six fold from the CYP1A2 promoter constructs. However, deletion of the PRB element did not affect the degree of activation by the c-Jun and the c-Fos. Therefore, it is unlikely that the c-Jun and the c-Fos activate the CYP1A2 promoter through this AP-1 consensus-like sequence in the PRB region.

• Clinical and Experimental Pediatrics
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• v.59 no.sup1
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• pp.29-31
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• 2016

Glucose transport 1 (GLUT-1) deficiency is a rare syndrome caused by mutations in the glucose transporter 1 gene (SLC2A1) and is characterized by early-onset intractable epilepsy, delayed development, and movement disorder. De novo mutations and several hot spots in N34, G91, R126, R153, and R333 of exons 2, 3, 4, and 8 of SLC2A1 are associated with this condition. Seizures, one of the main clinical features of GLUT-1 deficiency, usually develop during infancy. Most patients experience brief and subtle myoclonic jerk and focal seizures that evolve into a mixture of different types of seizures, such as generalized tonic-clonic, absence, myoclonic, and complex partial seizures. Here, we describe the case of a patient with GLUT-1 deficiency who developed infantile spasms and showed delayed development at 6 months of age. She had intractable epilepsy despite receiving aggressive antiepileptic drug therapy, and underwent a metabolic workup. Cerebrospinal fluid (CSF) examination showed CSF-glucose-to-blood-glucose ratio of 0.38, with a normal lactate level. Bidirectional sequencing of SLC2A1 identified a missense mutation (c.1198C>T) at codon 400 (p.Arg400Cys) of exon 9.

• Communications of the Korean Mathematical Society
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• v.11 no.1
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• pp.139-145
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• 1996

We show how some interesting results involving series summation and the digamma function are established by means of Riemann-Liouville operator of fractional calculus. We derive the relation $$ \frac{\Gamma(\lambda)}{\Gamma(\nu)} \sum^{\infty}_{n=1}{\frac{\Gamma(\nu+n)}{n\Gamma(\lambda+n)}_{p+2}F_{p+1}(a_1, \cdots, a_{p+1},\lambda + n; x/a)} = \sum^{\infty}_{k=0}{\frac{(a_1)_k \cdots (a_{(p+1)}{(b_1)_k \cdots (b_p)_k K!} (\frac{x}{a})^k [\psi(\lambda + k) - \psi(\lambda - \nu + k)]}, Re(\lambda) > Re(\nu) \geq 0 $$ and explain some special cases.

• Korean Journal of Mathematics
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• v.17 no.3
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• pp.271-281
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• 2009

We define injective and projective representations of a quiver $Q={\bullet}{\rightarrow}{\bullet}{\rightarrow}{\bullet}$. Then we show that a representation $M_1\longrightarrow[50]^{f1}M_2\longrightarrow[50]^{f2}M_3$ of a quiver $Q={\bullet}{\rightarrow}{\bullet}{\rightarrow}{\bullet}$ is projective if and only if each $M_1,\;M_2,\;M_3$ is projective left R-module and $f_1(M_1)$ is a summand of $M_2$ and $f_2(M_2)$ is a summand of $M_3$. And we show that a representation $M_1\longrightarrow[50]^{f1}M_2\longrightarrow[50]^{f2}M_3$ of a quiver $Q={\bullet}{\rightarrow}{\bullet}{\rightarrow}{\bullet}$ is injective if and only if each $M_1,\;M_2,\;M_3$ is injective left R-module and $ker(f_1)$ is a summand of $M_1$ and $ker(f_2)$ is a summand of $M_2$.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.16
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• pp.6923-6928
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• 2014

In recent years, mounting evidence has indicated that the CCND1 G870A gene polymorphism, which impacts the mitotic cell cycle, may influence leukemia or non-Hodgkin lymphoma risk. Unfortunately, the previous results were inconsistent. Therefore, a meta-analysis was performed to obtain a more precise estimation of any association. We conducted a search in PubMed, Embase and CNKI covering all published papers up to March, 2014. A total of 9 publications including 10 case-control studies met the inclusion criteria. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess association. The pooled ORs showed significant association in non-Hodgkin lymphoma (comparison A vs G: OR= 1.114, 95%CI=1.053-1.179, p=0.000; homozygote comparison AA vs GG: OR=1.245, 95%CI=1.110-1.396, p=0.000; heterozygote comparison AG vs GG: OR=1.095, 95%CI=1.000-1.199, p=0.05; dominant model AA/GA vs GG: OR=1.137, 95%CI=1.043-1.239, p=0.003; and recessive model AA vs GA/GG: OR=1.177, 95%CI=1.066-1.301, p=0.001). However, there was no association between the CCND1 G870A polymorphism and leukemia risk. In conclusion, the CCND1 G870A polymorphism may increase risk of non-Hodgkin lymphoma, but not leukemia. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with leukemia and non-Hodgkin lymphoma risk.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.8
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• pp.1176-1182
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• 2018

Objective: Progesterone receptor (PGR) and AT-rich interactive domain 1A (ARID1A) have important roles in the establishment and maintenance of pregnancy in the uterus. In present studies, we examined the expression of mitochondrial tumor suppressor 1 (MTUS1) in the murine uterus during early pregnancy as well as in response to ovarian steroid hormone treatment. Methods: We performed quantitative reverse transcription polymerase chain reaction and immunohistochemistry analysis to investigate the regulation of MTUS1 by ARID1A and determined expression patterns of MTUS1 in the uterus during early pregnancy. Results: The expression of MTUS1 was detected on day 0.5 of gestation (GD 0.5) and then gradually increased until GD 3.5 in the luminal and glandular epithelium. However, the expression of MTUS1 was significantly reduced in the uterine epithelial cells of $Pgr^{cre/+}Arid1a^{f/f}$ and Pgr knockout (PRKO) mice at GD 3.5. Furthermore, MTUS1 expression was remarkably induced after P4 treatment in the luminal and glandular epithelium of the wild-type mice. However, the induction of MTUS1 expression was not detected in uteri of $Pgr^{cre/+}Arid1a^{f/f}$ or PRKO mice treated with P4. Conclusion: These results suggest that MTUS1 is a novel target gene by ARID1A and PGR in the uterine epithelial cells.

• Journal of Microbiology
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• v.44 no.6
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• pp.641-648
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• 2006

We previously reported that Skp1, a component of the Skp1-Cullin-F-box protein (SCF) complex essential for the timely degradation of cell cycle proteins by ubiquitination, physically interacts with Bfa1, which is a key negative regulator of the mitotic exit network (MEN) in response to diverse checkpoint-activating stresses in budding yeast. In this study, we initially investigated whether the interaction of Skp1 and Bfa1 is involved in the regulation of the Bfa1 protein level during the cell cycle, especially by mediating its degradation. However, the profile of the Bfa1 protein did not change during the cell cycle in skp1-11, which is a SKP1 mutant allele in which the function of Skp1 as a part of SCF is completely impaired, thus indicating that Skp1 does not affect the degradation of Bfa1. On the other hand, we found that the skp1-12 mutant allele, previously reported to block G2-M transition, showed defects in mitotic exit and cytokinesis. The skp1-12 mutant allele also revealed a specific genetic interaction with ${\Delta}bfa1$. Bfa1 interacted with Skp1 via its 184 C-terminal residues (Bfa1-D8) that are responsible for its function in mitotic exit. In addition, the interaction between Bfa1 and the Skp1-12 mutant protein was stronger than that of Bfa1 and the wild type Skp1. We suggest a novel function of Skp1 in mitotic exit and cytokinesis, independent of its function as a part of the SCF complex. The interaction of Skp1 and Bfa1 may contribute to the function of Skp1 in the mitotic exit.

• Korean Journal of Crystallography
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• v.4 no.1
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• pp.6-10
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• 1993

11 β ,17 β -dihydroxy-9a-fluoro-l7a-methyl androst-4-en-3-one (Fluoxymesterone), CgoH29 FO,, orthorhombic, P2,2,2,, a=13.468(5) A, b= 19.554 (2)A, c=6.578(9)A, a=b=r=90˚, A (CuKa)=1.5406 A , Dm=1.289cm-3, Dc=1.299cm-3 and Z=4 at T=298k. The structure was solved by direct method using seminvariants of ggg Parity group and refined by the full-matrix least-square method, resulting model with reliability factor R=0.069 for 1098 unique reflection over 3σ . Ring A is an 1β-2a-half chair, 5 ring has a highly symmetrical chair conformation, C ring is in a distorted chair conformation and D ring is a 13aenveLope conformation. In the crystal structure, the molecules are packed with a hydrogen bond of 011-H23‥‥03(0.5+x, 1.5-y, 1.0-z) [1.94(9) A of H‥‥0.2.786(9)A of 0‥‥0 and 165(8) ˚ of

• Journal of applied mathematics & informatics
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• v.27 no.5_6
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• pp.1493-1499
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• 2009

Let $A_1$ and $A_2$ be nonzero complex idempotent and tripotent matrix, respectively. Denote a linear combination of the two matrices by A = $c_1A_1$ + $c_2A_2$, where $c_1,\;c_2$ are nonzero complex scalars. In this paper, under an assumption of $A_1A_2$ = $A_2A_1$, we characterize all situations in which the linear combination is tripotent. A statistical interpretation of this tripotent problem is also pointed out. Moreover, In [2], Baksalary characterized all situations in which the above linear combination is idem-potent by using the property of decomposition of a tripotent matrix, i.e. if $A_2$ is tripotent, then $A_2$ = $B_1-B_2$, where $B^2_i=B_i$, i = 1, 2 and $B_1B_2=B_2B_1=0$. While in this paper, by utilizing a method different from the one used by Baksalary in [2], we prove the theorem 1 in [2] again.

• Communications of the Korean Mathematical Society
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• v.18 no.4
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• pp.661-667
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• 2003

In this paper, we show, for a positive integer m and a large odd integer n, the polynomial equation (equation omitted) has a real zero on $((n+1)^{1+\frac{1}{m}},{\;}(n+1)^{1+\frac{1}{m}}+{\frac{1}{2}})$ and $((n+1)^{1+\frac{1}{m}}+{\frac{1}{2}},{\;}(n+2)^{1+\frac{1}{m}})$ respectively.