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991.
Fei Chen Fang Wang Hongyan Sun Yue Cai Weihua Mao Guoping Zhang Eva Vincze Feibo Wu 《Journal of Plant Growth Regulation》2010,29(4):394-408
A greenhouse hydroponic experiment was performed using Cd-sensitive (cv. Dong 17) and Cd-tolerant (Weisuobuzhi) barley seedlings
to evaluate how different genotypes responded to cadmium (Cd) toxicity in the presence of sodium nitroprusside (SNP), a nitric
oxide (NO) donor. Results showed that 5 μM Cd increased the accumulation of O2•−, H2O2, and malondialdehyde (MDA) but reduced plant height, chlorophyll content, net photosynthetic rate (P
n), and biomass, with a much more severe response in the Cd-sensitive genotype. Antioxidant enzyme activities increased significantly
under Cd stress in the roots of the tolerant genotype, whereas in leaves of the sensitive genotype, superoxide dismutase (SOD)
and ascorbate peroxide (APX), especially cytosol ascorbate peroxidase (cAPX), decreased after 5–15 days Cd exposure. Moreover,
Cd induces NO synthesis by stimulating nitrate reductase and nitric oxide synthetase-like enzymes in roots/leaves. A Cd-induced
NO transient increase in roots of the Cd-tolerant genotype might partly contribute to its Cd tolerance. Exogenous NO dramatically
alleviated Cd toxicity, markedly diminished Cd-induced reactive oxygen species (ROS) and MDA accumulation, ameliorated Cd-induced
damage to leaf/root ultrastructure, and increased chlorophyll content and P
n. External NO counteracted the pattern of alterations in certain antioxidant enzymes induced by Cd; for example, it significantly
elevated the depressed SOD, APX, and catalase (CAT) activities in the Cd-sensitive genotype after 10- and 15-day treatments.
Furthermore, NO significantly increased stromal APX and Mn-SOD activities in both genotypes and upregulated Cd-induced decrease
in cAPX activity and gene expression of root/leaf cAPX and leaf CAT1 in the Cd-sensitive genotype. These data suggest that under Cd stress, NO, as a potent antioxidant, protects barley seedlings
against oxidative damage by directly and indirectly scavenging ROS and helps to maintain stability and integrity of the subcellular
structure. 相似文献
992.
Can Wang Zengxia Li Zhaohua Yang Hongbo Zhao Yong Yang Kangli Chen Xiumei Cai Liying Wang Yinghong Shi Shuangjian Qiu Jia Fan Xiliang Zha 《Journal of cellular biochemistry》2010,109(1):113-123
N‐acetylglucosaminyltransferase V (GnT‐V) has been reported to be positively associated with tumor progression, but its mechanism still remains unknown. In the present study, we found that GnT‐V overexpression not only changed the glycosylation of receptor protein tyrosine phosphatase kappa (RPTPκ) but also decreased its protein level. Moreover, GnT‐V overexpression decreased cell calcium‐independent adhesion and increased the tyrosine phosphorylation level of β‐catenin, in which RPTPκ played an important role. Since RPTPκ has an RXKR motif, which is a favored cleavage site for furin, we used furin inhibitor to further explore the effect of RPTPκ on the change of cell adhesion and β‐catenin signaling induced by GnT‐V. Our results showed that preventing RPTPκ cleavage rescued the above effects of GnT‐V, suggesting that furin cleavage could be one of the factors for RPTPκ to regulate cell adhesion and β‐catenin signaling in GnT‐V overexpression cell lines. In addition, the increased tyrosine phosphorylation level of β‐catenin was associated with the increased nuclear level of β‐catenin and downstream signaling molecules such as c‐myc and cyclin D1 that were associated with cell proliferation. Our results suggest that GnT‐V could decrease human hepatoma SMMC‐7721 cell adhesion and promote cell proliferation partially through RPTPκ. J. Cell. Biochem. 109: 113–123, 2010. © 2009 Wiley‐Liss, Inc. 相似文献
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995.
转基因水稻外源基因的漂移研究 总被引:2,自引:0,他引:2
转基因水稻基因漂移可能带来环境安全性问题。利用农杆菌介导,把hpt基因转化水稻品种,通过后代筛选,以稳定遗传的含单拷贝转化株系为转基因花粉供体材料,研究转基因水稻向非转基因水稻不育系和常规稻(花粉受体)的外源基因漂移频率。结果表明,相邻种植时转基因水稻向雄性不育系品种的漂移频率为31.74%。随距离的增加漂移频率明显下降,在26m处仍能够检测到含外源基因个体的存在,并且在距离4m处出现一个漂移频率的升高;转基因水稻向常规品种的漂移频率则明显低于不育系,一般在2.0%以下,随距离的增加也呈现下降的趋势,在18m处开始无法检测到含外源基因的个体。 相似文献
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998.
Michal Hammel Yaping Yu Brandi L. Mahaney Brandon Cai Ruiqiong Ye Barry M. Phipps Robert P. Rambo Greg L. Hura Martin Pelikan Sairei So Ramin M. Abolfath David J. Chen Susan P. Lees-Miller John A. Tainer 《The Journal of biological chemistry》2010,285(2):1414-1423
DNA double strand break (DSB) repair by non-homologous end joining (NHEJ) is initiated by DSB detection by Ku70/80 (Ku) and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) recruitment, which promotes pathway progression through poorly defined mechanisms. Here, Ku and DNA-PKcs solution structures alone and in complex with DNA, defined by x-ray scattering, reveal major structural reorganizations that choreograph NHEJ initiation. The Ku80 C-terminal region forms a flexible arm that extends from the DNA-binding core to recruit and retain DNA-PKcs at DSBs. Furthermore, Ku- and DNA-promoted assembly of a DNA-PKcs dimer facilitates trans-autophosphorylation at the DSB. The resulting site-specific autophosphorylation induces a large conformational change that opens DNA-PKcs and promotes its release from DNA ends. These results show how protein and DNA interactions initiate large Ku and DNA-PKcs rearrangements to control DNA-PK biological functions as a macromolecular machine orchestrating assembly and disassembly of the initial NHEJ complex on DNA. 相似文献
999.
Sylvain Feliciangeli Magalie P. Tardy Guillaume Sandoz Franck C. Chatelain Richard Warth Jacques Barhanin Sa?d Bendahhou Florian Lesage 《The Journal of biological chemistry》2010,285(7):4798-4805
Tandem of P domains in a weak inwardly rectifying K+ channel 1 (TWIK1) is a K+ channel that produces unusually low levels of current. Replacement of lysine 274 by a glutamic acid (K274E) is associated with stronger currents. This mutation would prevent conjugation of a small ubiquitin modifier peptide to Lys-274, a mechanism proposed to be responsible for channel silencing. However, we found no biochemical evidence of TWIK1 sumoylation, and we showed that the conservative change K274R did not increase current, suggesting that K274E modifies TWIK1 gating through a charge effect. Now we rule out an eventual effect of K274E on TWIK1 trafficking, and we provide convincing evidence that TWIK1 silencing results from its rapid retrieval from the cell surface. TWIK1 is internalized via a dynamin-dependent mechanism and addressed to the recycling endosomal compartment. Mutation of a diisoleucine repeat located in its cytoplasmic C terminus (I293A,I294A) stabilizes TWIK1 at the plasma membrane, resulting in robust currents. The effects of I293A,I294A on channel trafficking and of K274E on channel activity are cumulative, promoting even more currents. Activation of serotoninergic receptor 5-HT1R or adrenoreceptor α2A-AR stimulates TWIK1 but has no effect on TWIK1I293A,I294A, suggesting that Gi protein activation is a physiological signal for increasing the number of active channels at the plasma membrane. 相似文献
1000.
Jennetta W. Hammond T. Lynne Blasius Virupakshi Soppina Dawen Cai Kristen J. Verhey 《The Journal of cell biology》2010,189(6):1013-1025
Long-distance transport in cells is driven by kinesin and dynein motors that move along microtubule tracks. These motors must be tightly regulated to ensure the spatial and temporal fidelity of their transport events. Transport motors of the kinesin-1 and kinesin-3 families are regulated by autoinhibition, but little is known about the mechanisms that regulate kinesin-2 motors. We show that the homodimeric kinesin-2 motor KIF17 is kept in an inactive state in the absence of cargo. Autoinhibition is caused by a folded conformation that enables nonmotor regions to directly contact and inhibit the enzymatic activity of the motor domain. We define two molecular mechanisms that contribute to autoinhibition of KIF17. First, the C-terminal tail interferes with microtubule binding; and second, a coiled-coil segment blocks processive motility. The latter is a new mechanism for regulation of kinesin motors. This work supports the model that autoinhibition is a general mechanism for regulation of kinesin motors involved in intracellular trafficking events. 相似文献