Contributors: Xu Jin-Wen, Li-Na Ding, Ning-Xi Zeng, Sui-Qing Chen, Shu-Hui Zheng, Hai-Mei Liu, RUN-MEI Li
... WB band
Contributors: José Augusto Morais de Andrade Jr
Contributors: Wei-hsiu Liu, Jang-Chun Lin, Jo-Ting Tsai, Tsu-Yi Chao, HSINI MA
... Left: Expression of MSI1, ICAM1, and LIN28 in GBM-U87MG/Ctrl, and GBM-U87MG/MSI1. Right: Expression of MSI1, ICAM1, and LIN28 in GBM-05MG/sh-Scr and GBM-05MG/sh-MSI1 cells. ß-actin was used as a loading control.
Data for: Marinitoga lauensis sp. nov., a novel deep-sea hydrothermal vent thermophilic anaerobic heterotroph with a prophage.
Contributors: anna-louise reysenbach, Lena Gouhier, Emily St. John
... Marinitoga lauensis sp. nov., a novel deep-sea hydrothermal vent thermophilic anaerobic heterotroph with a prophage. Stéphane L’Haridona*, Léna Gouhiera, Emily St. Johnb and Anna-Louise Reysenbachb Univ Brest, CNRS, IFREMER, Laboratoire de Microbiologie des Environnements Extrêmes, F-29280, Plouzané, Francea; Portland State University, Department of Biology and Center for Life in Extreme Environments, P.O. Box 751, Portland, OR 97207 USAb.
Contributors: Christopher Bretherton
... Map of collaborators
Data for: Seipin deletion in mice enhances phosphorylation and aggregation of tau protein through reduced neuronal PPARγ and insulin resistance
Contributors: Ling Chen
... We attached the independent replicates of Western blot analyses in the supplementary section that were used in various quantifications. The regions of line rectangles in these blots/gels, as representative images, were used in Figures of the main Text. In the Fig. 1e: the levels of hippocampal NF-H protein in seipin-sKO mice (sKO) and seipin-nKO mice (nKO) were lower than those of WT mice. In the Fig. 2a: the levels of tau protein in hippocampus of seipin-sKO mice, seipin-nKO mice and seipin-aKO mice (aKO) were not altered. In the Fig. 2b: the levels of oligomer tau protein were increased in seipin-sKO mice and seipin-nKO mice. In the Fig. 2c: the levels of hippocampal tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 were increased in seipin-sKO mice and seipin-nKO mic. In the Fig. 3a: the levels of PPARγ protein were decreased in hippocampus of seipin-sKO mice and seipin-nKO mice. In the Fig. 3b: the administration of PPARγ agonist rosiglitazone (rosi) for 7 days could correct the increased tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-sKO mice and seipin-nKO mice. In the Fig. 4a: seipin-sKO mice and seipin-nKO mice showed an increase in the GSK3β phosphorylation at Tyr21 and a decrease at Ser9, which were corrected by rosi. In the Fig. 4b: the treatment with AR-A014418 (AR) corrected the increased tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-nKO mice. In the Fig. 5a&5b: the phosphorylation of Akt and mTOR was elevated in seipin-sKO mice and seipin-nKO mice, which were corrected by rosi. In the Fig. 5c&5d: seipin-sKO mice and seipin-nKO mice showed a decrease in the ratio of LC3II/I and an elevation of p62 protein, which was rescued by the PI3K inhibitor LY294002 (LY) and mTOR inhibitor rapamycin (Rap), but not AR. In the Fig. 5e&5f: the administration of LY and Rap reduced the levels of oligomer tau protein and tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-nKO mice. In the Fig. 6c: the increased phosphorylation of JNK in seipin-sKO mice were corrected by treatment with rosi for 30 days. In the Fig. 6d: the P38 phosphorylation in seipin-sKO mice was not altered. In the Fig. 6e: the increased phosphorylation of tau at Ser396 in seipin-sKO mice was prevented by treatment with rosi for 30 days and the JNK inhibitor SP600125 (SP).
Data for: miR-196b inhibits cell proliferation, migration and invasion via MAP3K1 in hydatidiform mole
Contributors: Ying Kong, jia qi, na zou, yuefei xu, yunpeng xie, zhenzhen guo, linlin sui, Qiannan Sun Sun
... Raw data of western blot involved in the article
Contributors: Amin Namazi
... By review, both a basic knowledge of earth geology and with understanding In physics and chemistry, the law of conservation of energy, the basic fundamental of agriculture “It's Not the Harvest You Reap But the Seeds You Sow” so we should reach to the solution of the Earth-saving Method.
Targeted and persistent 8-oxoguanine base damage at telomeres promotes telomere loss and crisis. Fouquerel et al
Contributors: Patricia Opresko, Elise Fouquerel
... Telomeres are essential for genome stability. Oxidative stress caused by excess reactive oxygen species (ROS) accelerates telomere shortening. While telomeres are hypersensitive to ROS-mediated 8-oxoguanine (8-oxoG) formation, the biological impact of this common lesion at telomeres is poorly understood because ROS has pleiotropic effects. Here, we developed a chemoptogenetic tool that selectively produces 8-oxoG only at telomeres. Acute telomeric 8- oxoG formation increased telomere fragility in cells lacking OGG1, the enzyme that removes 8- oxoG, but did not compromise cell survival. However, chronic telomeric 8-oxoG induction over time shortens telomeres and impairs cell growth. Accumulation of telomeric 8-oxoG in chronically exposed OGG1 deficient cells triggers replication stress as evidenced by mitotic DNA synthesis at telomeres, and significantly increases telomere losses. These losses generate chromosome fusions, leading to chromatin bridges and micronuclei formation upon cell division. By confining base damage to the telomeres, we show that telomeric 8-oxoG accumulation directly drives telomere crisis.