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排序方式: 共有241条查询结果,搜索用时 15 毫秒
191.
A A 2-dimensional thin-layer method has been developed for the separation on cellulose of adenine and guanine derivatives. Using incubated rat cerebral cortex slices it was shown that noradrenaline and acetylcholine stimulated cAMP and cGMP production respectively but glutamate and gamma-aminobutyric acid stimulated production of both cyclic nucleotides. 相似文献
192.
We measured the carotid body volume of rats treated with chronic hypoxia alone and chronic hypoxia together with a single neonatal injection of N-ethyl-N-nitrosourea (10 mg/kg). All the animals so treated showed enlargement of their carotid bodies, but no carotid body chemodectomas occurred. 相似文献
193.
Hennies HC Kornak U Zhang H Egerer J Zhang X Seifert W Kühnisch J Budde B Nätebus M Brancati F Wilcox WR Müller D Kaplan PB Rajab A Zampino G Fodale V Dallapiccola B Newman W Metcalfe K Clayton-Smith J Tassabehji M Steinmann B Barr FA Nürnberg P Wieacker P Mundlos S 《Nature genetics》2008,40(12):1410-1412
Gerodermia osteodysplastica is an autosomal recessive disorder characterized by wrinkly skin and osteoporosis. Here we demonstrate that gerodermia osteodysplastica is caused by loss-of-function mutations in SCYL1BP1, which is highly expressed in skin and osteoblasts. The protein localizes to the Golgi apparatus and interacts with Rab6, identifying SCYL1BP1 as a golgin. These results associate abnormalities of the secretory pathway with age-related changes in connective tissues. 相似文献
194.
195.
Chambers JC Zhang W Sehmi J Li X Wass MN Van der Harst P Holm H Sanna S Kavousi M Baumeister SE Coin LJ Deng G Gieger C Heard-Costa NL Hottenga JJ Kühnel B Kumar V Lagou V Liang L Luan J Vidal PM Mateo Leach I O'Reilly PF Peden JF Rahmioglu N Soininen P Speliotes EK Yuan X Thorleifsson G Alizadeh BZ Atwood LD Borecki IB Brown MJ Charoen P Cucca F Das D de Geus EJ Dixon AL Döring A Ehret G Eyjolfsson GI Farrall M Forouhi NG Friedrich N Goessling W Gudbjartsson DF Harris TB Hartikainen AL Heath S 《Nature genetics》2011,43(11):1131-1138
Concentrations of liver enzymes in plasma are widely used as indicators of liver disease. We carried out a genome-wide association study in 61,089 individuals, identifying 42 loci associated with concentrations of liver enzymes in plasma, of which 32 are new associations (P = 10(-8) to P = 10(-190)). We used functional genomic approaches including metabonomic profiling and gene expression analyses to identify probable candidate genes at these regions. We identified 69 candidate genes, including genes involved in biliary transport (ATP8B1 and ABCB11), glucose, carbohydrate and lipid metabolism (FADS1, FADS2, GCKR, JMJD1C, HNF1A, MLXIPL, PNPLA3, PPP1R3B, SLC2A2 and TRIB1), glycoprotein biosynthesis and cell surface glycobiology (ABO, ASGR1, FUT2, GPLD1 and ST3GAL4), inflammation and immunity (CD276, CDH6, GCKR, HNF1A, HPR, ITGA1, RORA and STAT4) and glutathione metabolism (GSTT1, GSTT2 and GGT), as well as several genes of uncertain or unknown function (including ABHD12, EFHD1, EFNA1, EPHA2, MICAL3 and ZNF827). Our results provide new insight into genetic mechanisms and pathways influencing markers of liver function. 相似文献
196.
Van Houdt JK Nowakowska BA Sousa SB van Schaik BD Seuntjens E Avonce N Sifrim A Abdul-Rahman OA van den Boogaard MJ Bottani A Castori M Cormier-Daire V Deardorff MA Filges I Fryer A Fryns JP Gana S Garavelli L Gillessen-Kaesbach G Hall BD Horn D Huylebroeck D Klapecki J Krajewska-Walasek M Kuechler A Lines MA Maas S Macdermot KD McKee S Magee A de Man SA Moreau Y Morice-Picard F Obersztyn E Pilch J Rosser E Shannon N Stolte-Dijkstra I Van Dijck P Vilain C Vogels A Wakeling E Wieczorek D 《Nature genetics》2012,44(4):445-9, S1
197.
Sansone SA Rocca-Serra P Field D Maguire E Taylor C Hofmann O Fang H Neumann S Tong W Amaral-Zettler L Begley K Booth T Bougueleret L Burns G Chapman B Clark T Coleman LA Copeland J Das S de Daruvar A de Matos P Dix I Edmunds S Evelo CT Forster MJ Gaudet P Gilbert J Goble C Griffin JL Jacob D Kleinjans J Harland L Haug K Hermjakob H Ho Sui SJ Laederach A Liang S Marshall S McGrath A Merrill E Reilly D Roux M Shamu CE Shang CA Steinbeck C Trefethen A Williams-Jones B Wolstencroft K Xenarios I 《Nature genetics》2012,44(2):121-126
To make full use of research data, the bioscience community needs to adopt technologies and reward mechanisms that support interoperability and promote the growth of an open 'data commoning' culture. Here we describe the prerequisites for data commoning and present an established and growing ecosystem of solutions using the shared 'Investigation-Study-Assay' framework to support that vision. 相似文献
198.
Peacock CS Seeger K Harris D Murphy L Ruiz JC Quail MA Peters N Adlem E Tivey A Aslett M Kerhornou A Ivens A Fraser A Rajandream MA Carver T Norbertczak H Chillingworth T Hance Z Jagels K Moule S Ormond D Rutter S Squares R Whitehead S Rabbinowitsch E Arrowsmith C White B Thurston S Bringaud F Baldauf SL Faulconbridge A Jeffares D Depledge DP Oyola SO Hilley JD Brito LO Tosi LR Barrell B Cruz AK Mottram JC Smith DF Berriman M 《Nature genetics》2007,39(7):839-847
Leishmania parasites cause a broad spectrum of clinical disease. Here we report the sequencing of the genomes of two species of Leishmania: Leishmania infantum and Leishmania braziliensis. The comparison of these sequences with the published genome of Leishmania major reveals marked conservation of synteny and identifies only approximately 200 genes with a differential distribution between the three species. L. braziliensis, contrary to Leishmania species examined so far, possesses components of a putative RNA-mediated interference pathway, telomere-associated transposable elements and spliced leader-associated SLACS retrotransposons. We show that pseudogene formation and gene loss are the principal forces shaping the different genomes. Genes that are differentially distributed between the species encode proteins implicated in host-pathogen interactions and parasite survival in the macrophage. 相似文献
199.
Sebaihia M Wren BW Mullany P Fairweather NF Minton N Stabler R Thomson NR Roberts AP Cerdeño-Tárraga AM Wang H Holden MT Wright A Churcher C Quail MA Baker S Bason N Brooks K Chillingworth T Cronin A Davis P Dowd L Fraser A Feltwell T Hance Z Holroyd S Jagels K Moule S Mungall K Price C Rabbinowitsch E Sharp S Simmonds M Stevens K Unwin L Whithead S Dupuy B Dougan G Barrell B Parkhill J 《Nature genetics》2006,38(7):779-786
We determined the complete genome sequence of Clostridium difficile strain 630, a virulent and multidrug-resistant strain. Our analysis indicates that a large proportion (11%) of the genome consists of mobile genetic elements, mainly in the form of conjugative transposons. These mobile elements are putatively responsible for the acquisition by C. difficile of an extensive array of genes involved in antimicrobial resistance, virulence, host interaction and the production of surface structures. The metabolic capabilities encoded in the genome show multiple adaptations for survival and growth within the gut environment. The extreme genome variability was confirmed by whole-genome microarray analysis; it may reflect the organism's niche in the gut and should provide information on the evolution of virulence in this organism. 相似文献
200.
Park D Han CZ Elliott MR Kinchen JM Trampont PC Das S Collins S Lysiak JJ Hoehn KL Ravichandran KS 《Nature》2011,477(7363):220-224
Rapid and efficient removal of apoptotic cells by phagocytes is important during development, tissue homeostasis and in immune responses. Efficient clearance depends on the capacity of a single phagocyte to ingest multiple apoptotic cells successively, and to process the corpse-derived cellular material. However, the factors that influence continued clearance by phagocytes are not known. Here we show that the mitochondrial membrane potential of the phagocyte critically controls engulfment capacity, with lower potential enhancing engulfment and vice versa. The mitochondrial membrane protein Ucp2, which acts to lower the mitochondrial membrane potential, was upregulated in phagocytes engulfing apoptotic cells. Loss of Ucp2 reduced phagocytic capacity, whereas Ucp2 overexpression enhanced engulfment. Mutational and pharmacological studies indicated a direct role for Ucp2-mediated mitochondrial function in phagocytosis. Macrophages from Ucp2-deficient mice were impaired in phagocytosis in vitro, and Ucp2-deficient mice showed profound in vivo defects in clearing dying cells in the thymus and testes. Collectively, these data indicate that mitochondrial membrane potential and Ucp2 are key molecular determinants of apoptotic cell clearance. As Ucp2 is linked to metabolic diseases and atherosclerosis, this newly discovered role for Ucp2 in apoptotic cell clearance has implications for the complex aetiology and pathogenesis of these diseases. 相似文献