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저널/프로시딩 상세정보

권호별목차 / 소장처보기

H : 소장처정보

T : 목차정보

Experimental & molecular medicine : EMM 15건

  1. [국내논문]   Genotype-phenotype correlation of SMN locus genes in spinal muscular atrophy patients from India.  

    Kesari, Akanchha ; Idris, M Mohammed ; Chandak, Giri Raj ; Mittal, Balraj
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 147 - 154 , 2005 , 1226-3613 ,

    초록

    Spinal muscular atrophy has been classified into four groups based on the age of onset and clinical severity of the disease. Homozygous deletion in SMN1 gene causes the disease but the clinical severity may be modified by copy number of homologous gene SMN2 as well as the extent of deletion at SMN locus. In the view of scarcity of genotype and phenotype correlation data from India, this study has been undertaken to determine that correlation in SMA patients by using the SMN and NAIP genes and two polymorphic markers C212 and C272 located in this region. Two to four alleles of the markers C212 and C272 were observed in normal individuals. However, majority of Type I patients showed only one allele from both markers whereas in Type II and III patients, 2-3 alleles were observed. The SMN2 copy number in our type III patients showed that patients carry 3-5 copies of SMN2 gene. Our results suggest that extent of deletions encompassing H4F5, SMN1, NAIP and copy number of SMN2 gene can modify the SMA phenotype, thus accounting for the different clinical subtypes of the disease.

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  2. [국내논문]   Increased lysine N-methylation of a 23-kDa protein during hepatic regeneration.  

    Choi, Yong-Bock ; Ko, Myoung-Hyun ; Shin, Chang-Ho ; Kim, Kyung-Suk ; Hong, Kyeong-Man ; Paik, Moon-Kee ; Park, Dong-Eun
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 155 - 160 , 2005 , 1226-3613 ,

    초록

    The methylation of a 23-kDa nuclear protein increased after partial hepatectomy and methylation returned to basal levels after the initial stage of regeneration. The methylating enzyme was partially purified from rat liver by ammonium sulfate precipitation, DEAE-anion exchange chromatography and Butyl-Sepharose chromatography. The 23-kDa protein was purified from a nuclear fraction of liver tissue with SP-Sepharose. When the 23-kDa protein was methylated with the partially purified methyltransferase and analyzed on C(18) high performance liquid chromatography (HPLC), the methylated acceptor amino acid was monomethyl lysine (MML). Previously, only arginine N-methylation of specific substrate proteins has been reported during liver regeneration. However, in this report, we found that lysine N-methylation increased during early hepatic regeneration, suggesting that lysine N-methylation of the 23-kDa nuclear protein may play a functional role in hepatic regeneration. The methyltransferase did not methylate other proteins such as histones, hnRNPA1, or cytochrome C, suggesting the enzyme is a 23-kDa nuclear protein- specific lysine N-methyltransferase.

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  3. [국내논문]   Inositol 5'-phosphatase, SHIP1 interacts with phospholipase C-gamma1 and modulates EGF-induced PLC activity.  

    Song, Minseok ; Kim, Myung Jong ; Ha, Sanghoon ; Park, Jong Bae ; Ryu, Sung Ho ; Suh, Pann-Ghill
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 161 - 168 , 2005 , 1226-3613 ,

    초록

    Phospholipase C-gamma1, containing two SH2 and one SH3 domains which participate in the interaction between signaling molecules, plays a significant role in the growth factor-induced signal transduction. However, the role of the SH domains in the growth factor-induced PLC-gamma1 regulation is unclear. By peptide-mass fingerprinting analysis, we have identified SHIP1 as the binding protein for the SH3 domain of PLC-gamma1. SHIP1 was co-immunoprecipitated with PLC-gamma1 and potentiated EGF-induced PLC-gamma1 activation. However, inositol 5'-phosphatase activity of SHIP1 was not required for the potentiation of EGF-induced PLC-gamma1 activation. Taken together, these results suggest that SHIP1 may function as an adaptor protein which can potentiate EGF-induced PLC-gamma1 activation without regards to its inositol 5'-phosphatase activity.

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  4. [국내논문]   Modulation of the caveolin-3 and Akt status in caveolae by insulin resistance in H9c2 cardiomyoblasts.  

    Ha, Hyunil ; Pak, Yunbae
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 169 - 178 , 2005 , 1226-3613 ,

    초록

    We investigated glucose uptake and the translocation of Akt and caveolin-3 in response to insulin in H9c2 cardiomyoblasts exposed to an experimental insulin resistance condition of 100 nM insulin in a 25 mM glucose containing media for 24 h. The cells under the insulin resistance condition exhibited a decrease in insulin-stimulated 2-deoxy[(3)H]glucose uptake as compared to control cells grown in 5 mM glucose media. In addition to a reduction in insulin-induced Akt translocation to membranes, we observed a significant decrease in insulin-stimulated membrane association of phosphorylated Akt with a consequent increase of the cytosolic pool. Actin remodeling in response to insulin was also greatly retarded in the cells. When translocation of Akt and caveolin-3 to caveolae was examined, the insulin resistance condition attenuated localization of Akt and caveolin-3 to caveolae from cytosol. As a result, insulin-stimulated Akt activation in caveolae was significantly decreased. Taken together, our data indicate that the decrease of glucose uptake into the cells is related to their reduced levels of caveolin-3, Akt and phosphorylated Akt in caveolae. We conclude that the insulin resistance condition induced the retardation of their translocation to caveolae and in turn caused an attenuation in insulin signaling, namely activation of Akt in caveolae for glucose uptake into H9c2 cardiomyoblasts.

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  5. [국내논문]   15-Deoxy-delta12,14-PGJ2 inhibits IL-6-induced Stat3 phosphorylation in lymphocytes.  

    Kim, Hyo Jin ; Rho, Young Hee ; Choi, Seong Jai ; Lee, Young Ho ; Cheon, HyeonJoo ; Um, Jun Won ; Sohn, Jeongwon ; Song, Gwan Gyu ; Ji, Jong Dae
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 179 - 185 , 2005 , 1226-3613 ,

    초록

    15-deoxy-delta(12,14)-PGJ(2)(15d-PGJ(2)) is a natural ligand that activates the peroxisome proliferators-activated receptor (PPAR) gamma, a member of nuclear receptor family implicated in regulation of lipid metabolism and adipocyte differentiation. Recent studies have shown that 15d-PGJ(2) is the potent anti-inflammatory agent functioning via PPARgamma-dependent and -independent mechanisms. Most postulated mechanisms for anti-inflammatory action of PPARgamma agonists are involved in inhibiting NF-kappaB signaling pathway. We examined the possibility that IL-6 signaling via the Jak-Stat pathway is modulated by 15d-PGJ(2) in lymphocytes and also examined whether the inhibition of IL-6 signaling is dependent of PPARgamma. 15d-PGJ(2) blocked IL-6 induced Stat1 and Stat3 activation in primary human lymphocytes, Jurkat cells and immortalized rheumatoid arthritis B cells. Inhibition of IL-6 signaling was induced rapidly within 15 min after treatment of 15d-PGJ(2). Other PPARgamma-agonists, such as troglitazone and ciglitazone, did not inhibit IL-6 signaling, indicating that 15d-PGJ(2) affect the IL-6-induced Jak-Stat signaling pathway via PPARgamma-independent mechanism. Although cycloheximide reversed 15d-PGJ(2)-mediated inhibition of Stat3 activation, actinomycin D had no effect on 15d-PGJ(2)-mediated inhibition of IL-6 signaling, indicating that inhibition of IL-6 signaling occur independent of de novo gene expression. These results show that 15d-PGJ(2) specifically inhibit Jak-Stat signaling pathway in lymphocytes, and suggest that 15d-PGJ(2) may regulate inflammatory reactions through the modulation of different signaling pathway other than NF-kappaB in lymphocytes.

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  6. [국내논문]   Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets.  

    Cho, Jae-We ; Park, Kun ; Kweon, Gi Ryang ; Jang, Byeong-Churl ; Baek, Won-Ki ; Suh, Min-Ho ; Kim, Chang-Wook ; Lee, Kyu-Suk ; Suh, Seong-Il
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 186 - 192 , 2005 , 1226-3613 ,

    초록

    Ultraviolet B (UVB) irradiation of skin induces an acute inflammation. Cyclooxygenase-2 (COX-2) protein plays key roles in acute inflammation in UVB-irradiated keratinocyte cell line HaCaT. Recently, curcumin has been regarded as a promising anti-inflammatory agent due to its ability to inhibit COX-2 expression. However, it remains largely unknown whether curcumin inhibits the UVB-induced COX-2 expression in HaCaT cells. This study was undertaken to clarify the effect of curcumin on the expression of COX-2 in UVB- irradiated HaCaT cells and further determined the molecular mechanisms associated with this process. In this study, we have found that the expression of COX-2 mRNA and protein were up-regulated in UVB-irradiated HaCaT cells in a dose- and time-dependent manner. Interestingly, treatment with curcumin strongly inhibited COX-2 mRNA and protein expressions in UVB-irradiated HaCaT cells. Notably, there was effective inhibition by curcumin on UVB-induced activations of p38 MAPK and JNK in HaCaT cells. The DNA binding activity of AP-1 transcription factor was also markedly decreased with curcumin treatment in UVB-irradiated HaCaT cells. These results collectively suggest that curcumin may inhibit COX- 2 expression by suppressing p38 MAPK and JNK activities in UVB-irradiated HaCaT cells. We propose that curcumin may be applied as an effective and novel sunscreen drug for the protection of photoinflammation.

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  7. [국내논문]   In vivo ligation of glucocorticoid-induced TNF receptor enhances the T-cell immunity to herpes simplex virus type 1.  

    La, Soojin ; Kim, Eunhwa ; Kwon, Byungsuk
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 193 - 198 , 2005 , 1226-3613 ,

    초록

    GITR (glucocorticoid-induced TNF receptor) is a recently identified member of the TNF receptor superfamily. The receptor is preferentially expressed on CD4(+)CD25(+) regulatory T cells and GITR signals break the suppressive activity of the subset. In this study, we wanted to reveal the in vivo function of GITR in herpes simplex virus type 1 (HSV-1) infection. A single injection of anti-GITR mAb (DTA-1) immediately after viral infection significantly increased the number of CD4(+) and CD8(+) T cells expressing CD25, an activation surface marker, and secreting IFN-gamma. We confirmed these in vivo observations by showing ex vivo that re-stimulation of CD4(+) or CD8(+) T cells with a CD4(+) or CD8(+) T-cell-specific HSV-1 peptide, respectively, induced a significant elevation in cell proliferation and in IFN-gamma secretion. Our results indicate that GITR signals play a critical role in the T-cell immunity to HSV-1.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  8. [국내논문]   COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway in human bladder cancer cells.  

    Choi, Eun-Mi ; Kwak, Sahng-June ; Kim, Young-Myeong ; Ha, Kwon-Soo ; Kim, Jong-Il ; Lee, Sam W ; Han, Jeong A
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 199 - 203 , 2005 , 1226-3613 ,

    초록

    Cyclooxygenase-2 (COX-2) has been reported to be associated with tumor development and progression as well as to protect cells from apoptosis induced by various cellular stresses. Through a tetracycline-regulated COX-2 overexpression system, we found that COX-2 inhibits detachment-induced apoptosis (anoikis) in a human bladder cancer cell line, EJ. We also found that the inhibition of anoikis by COX-2 results from activation of the PI-3K/Akt pathway as evidenced by suppression of the COX-2 effect on anoikis by a PI-3K inhibitor, LY294002. Furthermore, COX-2 enhanced Mcl-1 expression in the anoikis process, implying that Mcl-1 also may be involved in mediating the survival function of COX-2. Together, these results suggest that COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway and probably by enhancement of Mcl-1 expression in human bladder cancer cells. This anti- anoikis effect of COX-2 may be a part of mechanisms to promote tumor development and progression.

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  9. [국내논문]   Co-localization and interaction of organic anion transporter 1 with caveolin-2 in rat kidney.  

    Kwak, Jin-Oh ; Kim, Hyun-Woo ; Oh, Kwang-Jin ; Kim, Dong Su ; Han, Ki Ok ; Cha, Seok Ho
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 204 - 212 , 2005 , 1226-3613 ,

    초록

    The organic anion transporters (OAT) have recently been identified. Although the some transport properties of OATs in the kidney have been verified, the regulatory mechanisms for OAT's functions are still not fully understood. The rat OAT1 (rOAT1) transports a number of negatively charged organic compounds between the cells and their extracellular milieu. Caveolin (Cav) also plays a role in membrane transport. Therefore, we investigated the protein-protein interactions between rOAT1 and caveolin-2. In the rat kidney, the expressions of rOAT1 mRNA and protein were observed in both the cortex and the outer medulla. With respect to Cav-2, the expressions of mRNA and protein were observed in all portions of the kidney (cortex

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  10. [국내논문]   Presence of autocrine hepatocyte growth factor-Met signaling and its role in proliferation and migration of SNU-484 gastric cancer cell line.  

    Park, Minseon ; Park, Hyelee ; Kim, Wook-Hwan ; Cho, Hyeseong ; Lee, Jae-Ho
    Experimental & molecular medicine : EMM v.37 no.3 ,pp. 213 - 219 , 2005 , 1226-3613 ,

    초록

    Autocrine stimulation via coexpression of hepatocyte growth factor (HGF) and its receptor (Met) has been reported in many human sarcomas, but few in carcinomas. In this report, we found that one gastric cancer cell line, SNU-484, among 11 gastric cell lines tested has an autocrine HGF- Met stimulation. RT-PCR, ELISA and scattering assay using MDCK cells revealed that SNU-484 cells secreted a significant amount of active HGF (about 1.25 +/- 0.41 ng/24 h/10(6) cells) into conditioned medium. Resultantly, Met in this cell line was constitutively phosphorylated. Neutralizing antibodies against HGF reduced the tyrosine phosphorylation of Met, resulting in the inhibition of cell proliferation and migration (P

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