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31.
Evidence of independent gene duplications during the evolution of archaeal and eukaryotic family B DNA polymerases 总被引:1,自引:0,他引:1
Eukaryotes and archaea both possess multiple genes coding for family B DNA
polymerases. In animals and fungi, three family B DNA polymerases, alpha,
delta, and epsilon, are responsible for replication of nuclear DNA. We used
a PCR-based approach to amplify and sequence phylogenetically conserved
regions of these three DNA polymerases from Giardia intestinalis and
Trichomonas vaginalis, representatives of early-diverging eukaryotic
lineages. Phylogenetic analysis of eukaryotic and archaeal paralogs
suggests that the gene duplications that gave rise to the three replicative
paralogs occurred before the divergence of the earliest eukaryotic
lineages, and that all eukaryotes are likely to possess these paralogs. One
eukaryotic paralog, epsilon, consistently branches within archaeal
sequences to the exclusion of other eukaryotic paralogs, suggesting that an
epsilon-like family B DNA polymerase was ancestral to both archaea and
eukaryotes. Because crenarchaeote and euryarchaeote paralogs do not form
monophyletic groups in phylogenetic analysis, it is possible that archaeal
family B paralogs themselves evolved by a series of gene duplications
independent of the gene duplications that gave rise to eukaryotic paralogs.
相似文献
32.
Macrophage-mediated suppression of con A-induced IL-2 production in spleen cells from syphilitic rabbits 总被引:11,自引:0,他引:11
M A Tomai B J Elmquist S M Warmka T J Fitzgerald 《Journal of immunology (Baltimore, Md. : 1950)》1989,143(1):309-314
Blast transformation studies have indicated a diminished T cell response in spleen cell preparations from rabbits infected with Treponema pallidum. IL-2 synthesis by T lymphocytes is required for proliferation of these cells. Thus, Con A-induced IL-2 generation was measured in syphilitic animals infected for 9 to 14 days. IL-2 production in the infected rabbits was only one-half that observed for uninfected rabbits. This marked decrease in IL-2 was not caused by decreased IL-1 secretion by adherent cells from infected animals because similar levels were found in both infected and uninfected splenic cultures. This decrease was also not caused by an increase in infected spleen cell adsorption of IL-2; similar numbers of receptors for this IL were present in Con A-stimulated infected and uninfected splenic preparations. The inhibited IL-2 production in infected spleen cells was reversed upon removal of the adherent cells and also elevated upon addition of indomethacin to the cultures. PGE levels were also elevated in splenic cultures from infected animals. Finally, IL-2 synthesis, when evaluated at various days postinfection, showed that at 4 days, splenic cells generated twice as much IL-2 as uninfected cells. At 9 to 14 days, IL-2 levels were dramatically decreased (50% lower than that observed in uninfected cultures), and suppression of IL-2 by adherent cells was observed as late as 35 days post-infection. We propose that premature down regulation (suppression) of IL-2 secretion is mediated by adherent cells via a cyclo-oxygenase product, most likely PGE. These results may explain why most, but not all, treponemes are cleared during infection, and why the secondary manifestations of the disease occur. 相似文献
33.
Relatively little is known about the mechanisms that link changing levels of glucose and neuronal activity. A paper in the current issue of Neuron by Burdakov et al. demonstrates that orexin/hypocretin neurons are inhibited by rising glucose in part due to membrane potential effects mediated by tandem-pore K(+) (K(2P)) channels. The findings may shed light on the mechanisms that link hypoglycemia and coordinated arousal and autonomic responses. 相似文献
34.
Heisler LK Jobst EE Sutton GM Zhou L Borok E Thornton-Jones Z Liu HY Zigman JM Balthasar N Kishi T Lee CE Aschkenasi CJ Zhang CY Yu J Boss O Mountjoy KG Clifton PG Lowell BB Friedman JM Horvath T Butler AA Elmquist JK Cowley MA 《Neuron》2006,51(2):239-249
The neural pathways through which central serotonergic systems regulate food intake and body weight remain to be fully elucidated. We report that serotonin, via action at serotonin1B receptors (5-HT1BRs), modulates the endogenous release of both agonists and antagonists of the melanocortin receptors, which are a core component of the central circuitry controlling body weight homeostasis. We also show that serotonin-induced hypophagia requires downstream activation of melanocortin 4, but not melanocortin 3, receptors. These results identify a primary mechanism underlying the serotonergic regulation of energy balance and provide an example of a centrally derived signal that reciprocally regulates melanocortin receptor agonists and antagonists in a similar manner to peripheral adiposity signals. 相似文献
35.
By locally infecting epididymal adipocytes of obese diabetic mice with the uncoupling protein-1 transgene, Yamada et al. (2006[this issue of Cell Metabolism]) unexpectedly induce leptin sensitivity with hypophagia and improvement in abnormal glucose and lipid abnormalities. 相似文献
36.
Jeroen CW Rijk Ad ACM Peijnenburg Peter JM Hendriksen Johan M Van Hende Maria J Groot Michel WF Nielen 《BMC veterinary research》2010,6(1):44
Background
Within the European Union the use of growth promoting agents in animal production is prohibited. Illegal use of natural prohormones like dehydroepiandrosterone (DHEA) is hard to prove since prohormones are strongly metabolized in vivo. In the present study, we investigated the feasibility of a novel effect-based approach for monitoring abuse of DHEA. Changes in gene expression profiles were studied in livers of bull calves treated orally (PO) or intramuscularly (IM) with 1000 mg DHEA versus two control groups, using bovine 44K DNA microarrays. In contrast to controlled genomics studies, this work involved bovines purchased at the local market on three different occasions with ages ranging from 6 to 14 months, thereby reflecting the real life inter-animal variability due to differences in age, individual physiology, season and diet. 相似文献37.
38.
Rethinking the central causes of diabetes 总被引:5,自引:0,他引:5
39.
Leptin receptor signaling in POMC neurons is required for normal body weight homeostasis 总被引:21,自引:0,他引:21
Balthasar N Coppari R McMinn J Liu SM Lee CE Tang V Kenny CD McGovern RA Chua SC Elmquist JK Lowell BB 《Neuron》2004,42(6):983-991
Neuroanatomical and electrophysiological studies have shown that hypothalamic POMC neurons are targets of the adipostatic hormone leptin. However, the physiological relevance of leptin signaling in these neurons has not yet been directly tested. Here, using the Cre/loxP system, we critically test the functional importance of leptin action on POMC neurons by deleting leptin receptors specifically from these cells in mice. Mice lacking leptin signaling in POMC neurons are mildly obese, hyperleptinemic, and have altered expression of hypothalamic neuropeptides. In summary, leptin receptors on POMC neurons are required but not solely responsible for leptin's regulation of body weight homeostasis. 相似文献
40.
Leland S. Hu Shuluo Ning Jennifer M. Eschbacher Nathan Gaw Amylou C. Dueck Kris A. Smith Peter Nakaji Jonathan Plasencia Sara Ranjbar Stephen J. Price Nhan Tran Joseph Loftus Robert Jenkins Brian P. O’Neill William Elmquist Leslie C. Baxter Fei Gao David Frakes John P. Karis Christine Zwart Kristin R. Swanson Jann Sarkaria Teresa Wu J. Ross Mitchell Jing Li 《PloS one》2015,10(11)