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991.
992.
Jung Dae Lim Jung-Il Cho Youn-Il Park Tae-Ryong Hahn Sang-Bong Choi Jong-Seong Jeon 《Physiologia plantarum》2006,126(4):572-584
In many higher plants, sucrose is loaded as a major carbon photoassimiliate into the phloem apoplastically by sucrose transporters (SUTs) and unloaded in sink tissues, where it serves as a storage material, carbohydrate backbone, and energy source. In sink tissues, a proportion of sucrose molecules are converted by cell wall invertases (CINs) into hexose that is imported into cells by monosaccharide transporters (MSTs). Thus, in developing seeds, co-ordinated regulation of SUTs, CINs, and MSTs is crucial in carbon distribution. Here, we summarize current efforts on the identification of SUTs, CINs, and MSTs in rice. 相似文献
993.
Yun Hwa Hong Ji Young Kim Jeong Ho Lee† Hong Gu Chae Sung Soo Jang Ju Hong Jeon Chul Hoon Kim† Jun Kim Sang Jeong Kim‡ 《Journal of neurochemistry》2009,111(1):61-71
Agonist-induced internalization of metabotropic glutamate receptors (mGluRs) plays an important role in neuronal signaling. Although internalization of mGluRs has been reported to be mediated by clathrin-dependent pathway, studies describing clathrin-independent pathways are emerging. Here, we report that agonist-induced internalization of mGluR1α is mediated by caveolin. We show that two caveolin-binding motifs of mGluR1α interact with caveolin1/2. Using cell surface-immunoprecipitation and total internal reflection fluorescence imaging, we found that agonist-induced internalization of mGluR1α is regulated by caveolin-binding motifs of the receptor in heterologous cells. Moreover, in the cerebellum, group I mGluR agonist dihydroxyphenylglycol increased the interaction of phosphorylated caveolin with mGluR1α. This interaction was blocked by methyl-β-cyclodextrin, known to disrupt caveolin/caveolae-dependent signaling by cholesterol depletion. Methyl-β-cyclodextrin also blocked the agonist-induced internalization of mGluR1α. Thus, these findings represent the evidence for agonist-induced internalization of mGluR1α via caveolin and suggest that caveolin might play a role in synaptic metaplasticity by regulating internalization of mGluR1α in the cerebellum. 相似文献
994.
Shin DM Jeon BY Lee HM Jin HS Yuk JM Song CH Lee SH Lee ZW Cho SN Kim JM Friedman RL Jo EK 《PLoS pathogens》2010,6(12):e1001230
The "enhanced intracellular survival" (eis) gene of Mycobacterium tuberculosis (Mtb) is involved in the intracellular survival of M. smegmatis. However, its exact effects on host cell function remain elusive. We herein report that Mtb Eis plays essential roles in modulating macrophage autophagy, inflammatory responses, and cell death via a reactive oxygen species (ROS)-dependent pathway. Macrophages infected with an Mtb eis-deletion mutant H37Rv (Mtb-Δeis) displayed markedly increased accumulation of massive autophagic vacuoles and formation of autophagosomes in vitro and in vivo. Infection of macrophages with Mtb-Δeis increased the production of tumor necrosis factor-α and interleukin-6 over the levels produced by infection with wild-type or complemented strains. Elevated ROS generation in macrophages infected with Mtb-Δeis (for which NADPH oxidase and mitochondria were largely responsible) rendered the cells highly sensitive to autophagy activation and cytokine production. Despite considerable activation of autophagy and proinflammatory responses, macrophages infected with Mtb-Δeis underwent caspase-independent cell death. This cell death was significantly inhibited by blockade of autophagy and c-Jun N-terminal kinase-ROS signaling, suggesting that excessive autophagy and oxidative stress are detrimental to cell survival. Finally, artificial over-expression of Eis or pretreatment with recombinant Eis abrogated production of both ROS and proinflammatory cytokines, which depends on the N-acetyltransferase domain of the Eis protein. Collectively, these data indicate that Mtb Eis suppresses host innate immune defenses by modulating autophagy, inflammation, and cell death in a redox-dependent manner. 相似文献
995.
Jeon KI Jono H Miller CL Cai Y Lim S Liu X Gao P Abe J Li JD Yan C 《The FEBS journal》2010,277(24):5026-5039
The phenotypic change of vascular smooth muscle cells (VSMCs), from a 'contractile' phenotype to a 'synthetic' phenotype, is crucial for pathogenic vascular remodeling in vascular diseases such as atherosclerosis and restenosis. Ca(2+)/calmodulin-stimulated phosphodiesterase 1 (PDE1) isozymes, including PDE1A and PDE1C, play integral roles in regulating the proliferation of synthetic VSMCs. However, the underlying molecular mechanism(s) remain unknown. In this study, we explore the role and mechanism of PDE1 isoforms in regulating β-catenin/T-cell factor (TCF) signaling in VSMCs, a pathway important for vascular remodeling through promoting VSMC growth and survival. We found that inhibition of PDE1 activity markedly attenuated β-catenin/TCF signaling by downregulating β-catenin protein. The effect of PDE1 inhibition on β-catenin protein reduction is exerted via promoting glycogen synthase kinase 3 (GSK3)β activation, β-catenin phosphorylation and subsequent β-catenin protein degradation. Moreover, PDE1 inhibition specifically upregulated phosphatase protein phosphatase 2A (PP2A) B56γ subunit gene expression, which is responsible for the effects of PDE1 inhibition on GSK3β and β-catenin/TCF signaling. Furthermore, the effect of PDE1 inhibition on β-catenin was specifically mediated by PDE1A but not PDE1C isozyme. Interestingly, in synthetic VSMCs, PP2A B56γ, phospho-GSK3β and phospho-β-catenin were all found in the nucleus, suggesting that PDE1A regulates nuclear β-catenin protein stability through the nuclear PP2A-GSK3β-β-catenin signaling axis. Taken together, these findings provide direct evidence for the first time that PP2A B56γ is a critical mediator for PDE1A in the regulation of β-catenin signaling in proliferating VSMCs. 相似文献
996.
Chang-Hyo Goh Kouji Satoh Shoshi Kikuchi Seong-Cheol Kim Suk-Min Ko Hong-Gyu Kang Jong-Seong Jeon Cheol Soo Kim Youn-Il Park 《Plant biotechnology reports》2010,4(4):281-291
The rice CHLH gene encodes the Mg2+-chelatase H subunit, which is involved in chlorophyll biosynthesis. Growth of the chlorophyll-deficient oschlh mutant is supported by mitochondrial activity. In this study, we investigated the activity of mitochondrial respiration in
the illuminated leaves during oschlh seedling development. Growth of mutant plants was enhanced in the presence of 3% sucrose, which may be used by mitochondria
to meet cellular energy requirements. ATP content in these mutants was, however, significantly lowered in light conditions.
Low cytosolic levels of NADH in illuminated oschlh mutant leaves further indicated the inhibition of mitochondrial metabolism. This down-regulation was particularly evident
for oxidative stress-responsive genes in the mutant under light conditions. Hydrogen peroxide levels were higher in oschlh mutant leaves than in wild-type leaves; this increase was largely caused by the impairment of the expression of the antioxidant
genes, such as OsAPX1, OsRAC1, and OsAOXc in knockout plants. Moreover, treatment of mesophyll protoplasts with ascorbic acid or catalase recovered ATP content in
the mutants. Taken together, these results suggest that the light-mediated inhibition of mitochondrial activity leads to stunted
growth of CHLH rice seedlings. 相似文献
997.
Nonalcoholic fatty liver disease (NAFLD) is highly prevalent and associated with considerable morbidities. Unfortunately, there is no currently available drug established to treat NAFLD. It was recently reported that intraperitoneal administration of taurine-conjugated ursodeoxycholic acid (TUDCA) improved hepatic steatosis in ob/ob mice. We hereby examined the effect of oral TUDCA treatment on hepatic steatosis and associated changes in hepatic gene expression in ob/ob mice. We administered TUDCA to ob/ob mice at a dose of 500 mg/kg twice a day by gastric gavage for 3 weeks. Body weight, glucose homeostasis, endoplasmic reticulum (ER) stress, and hepatic gene expression were examined in comparison with control ob/ob mice and normal littermate C57BL/6J mice. Compared to the control ob/ob mice, TUDCA treated ob/ob mice revealed markedly reduced liver fat stained by oil red O (44.2±5.8% vs. 21.1±10.4%, P<0.05), whereas there was no difference in body weight, oral glucose tolerance, insulin sensitivity, and ER stress. Microarray analysis of hepatic gene expression demonstrated that oral TUDCA treatment mainly decreased the expression of genes involved in de novo lipogenesis among the components of lipid homeostasis. At pathway levels, oral TUDCA altered the genes regulating amino acid, carbohydrate, and drug metabolism in addition to lipid metabolism. In summary, oral TUDCA treatment decreased hepatic steatosis in ob/ob mice by cooperative regulation of multiple metabolic pathways, particularly by reducing the expression of genes known to regulate de novo lipogenesis. 相似文献
998.
Background
Organisms, at scales ranging from unicellular to mammals, have been known to exhibit foraging behavior described by random walks whose segments confirm to Lévy or exponential distributions. For the first time, we present evidence that single cells (mammary epithelial cells) that exist in multi-cellular organisms (humans) follow a bimodal correlated random walk (BCRW).Methodology/Principal Findings
Cellular tracks of MCF-10A pBabe, neuN and neuT random migration on 2-D plastic substrates, analyzed using bimodal analysis, were found to reveal the BCRW pattern. We find two types of exponentially distributed correlated flights (corresponding to what we refer to as the directional and re-orientation phases) each having its own correlation between move step-lengths within flights. The exponential distribution of flight lengths was confirmed using different analysis methods (logarithmic binning with normalization, survival frequency plots and maximum likelihood estimation).Conclusions/Significance
Because of the presence of non-uniform turn angle distribution of move step-lengths within a flight and two different types of flights, we propose that the epithelial random walk is a BCRW comprising of two alternating modes with varying degree of correlations, rather than a simple persistent random walk. A BCRW model rather than a simple persistent random walk correctly matches the super-diffusivity in the cell migration paths as indicated by simulations based on the BCRW model. 相似文献999.
Chan‐Young Jeon Hee‐Jun Kim Hiroshi Morii Nozomu Mori Jeffrey Settleman Jae‐Yong Lee Jaebong Kim Sung‐Chan Kim Jae‐Bong Park 《Journal of cellular physiology》2010,224(3):786-794
The rat pheochromocytoma cell line PC12 has been widely used as a model to study neuronal differentiation. PC12 cells give rise to neurites in response to basic fibroblast growth factor (bFGF). However, it is unclear whether bFGF promotes neurite outgrowth by inducing RhoA inactivation, and a mechanism for RhoA inactivation in PC12 cells in response to bFGF has not been reported. Lysophosphatidic acid (LPA) treatment and the expression of constitutively active (CA)‐RhoA (RhoA V14) impaired neurite formation in response to bFGF, while Tat‐C3 exoenzyme and the expression of dominant negative (DN)‐RhoA (RhoA N19) stimulated neurite outgrowth. GTP‐bound RhoA levels were reduced in response to bFGF, which suggests that the inactivation of RhoA is essential to neurite outgrowth in response to bFGF. To investigate the mechanism of RhoA inactivation, this study examined the roles of p190RhoGAP and Rap‐dependent RhoGAP (ARAP3). DN‐p190RhoGAP prevented neurite outgrowth, while WT‐p190RhoGAP and Src synergistically stimulated neurite outgrowth; these findings suggest that bFGF promotes the inactivation of RhoA and subsequent neurite outgrowth through p190RhoGAP and Src. Furthermore, DN‐Rap1 and DN‐ARAP3 reduced neurite formation in PC12 cells. These results suggest that RhoA is likely to be inactivated by p190RhoGAP and ARAP3 during neurite outgrowth in response to bFGF. J. Cell. Physiol. 224: 786–794, 2010. © 2010 Wiley‐Liss, Inc. 相似文献
1000.
Sunggeon Ko Gil Bu Kang Sung Min Song Jung-Gyu Lee Dong Yeon Shin Ji-Hye Yun Yi Sheng Chaejoon Cheong Young Ho Jeon Yong-Keun Jung Cheryl H. Arrowsmith George V. Avvakumov Sirano Dhe-Paganon Yung Joon Yoo Soo Hyun Eom Weontae Lee 《The Journal of biological chemistry》2010,285(46):36070-36080
E2–25K/Hip2 is an unusual ubiquitin-conjugating enzyme that interacts with the frameshift mutant of ubiquitin B (UBB+1) and has been identified as a crucial factor regulating amyloid-β neurotoxicity. To study the structural basis of the neurotoxicity mediated by the E2–25K-UBB+1 interaction, we determined the three-dimensional structures of UBB+1, E2–25K and the E2–25K/ubiquitin, and E2–25K/UBB+1 complex. The structures revealed that ubiquitin or UBB+1 is bound to E2–25K via the enzyme MGF motif and residues in α9 of the enzyme. Polyubiquitylation assays together with analyses of various E2–25K mutants showed that disrupting UBB+1 binding markedly diminishes synthesis of neurotoxic UBB+1-anchored polyubiquitin. These results suggest that the interaction between E2–25K and UBB+1 is critical for the synthesis and accumulation of UBB+1-anchored polyubiquitin, which results in proteasomal inhibition and neuronal cell death. 相似文献