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1.
During serial structure analysis of cobaloxime derivatives, aimed at interpreting the catalytic capability of the asymmetric hydrogenation, we have found that the crystal of R-alpha-cyanoethyl (S-alpha-methylbenzylamine)-cobaloxime changes its unit cell dimensions by X-ray exposure without degradation of a single crystal form. The rate of the change was so slow that it was possible to collect the intensity data for several intermediate stages. We have proved, by calculating electron density in each stage, that the change reflects the racemisation of the cyanoethyl group. 相似文献
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Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence 总被引:46,自引:0,他引:46
Ohtani N Zebedee Z Huot TJ Stinson JA Sugimoto M Ohashi Y Sharrocks AD Peters G Hara E 《Nature》2001,409(6823):1067-1070
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ICOS is essential for effective T-helper-cell responses 总被引:60,自引:0,他引:60
Tafuri A Shahinian A Bladt F Yoshinaga SK Jordana M Wakeham A Boucher LM Bouchard D Chan VS Duncan G Odermatt B Ho A Itie A Horan T Whoriskey JS Pawson T Penninger JM Ohashi PS Mak TW 《Nature》2001,409(6816):105-109
The outcome of T-cell responses after T-cell encounter with specific antigens is modulated by co-stimulatory signals, which are required for both lymphocyte activation and development of adaptive immunity. ICOS, an inducible co-stimulator with homology to CD28, is expressed on activated, but not resting T cells, and shows T-cell co-stimulatory function in vitro. ICOS binds specifically to its counter-receptor B7RP-1 (refs 5,6,7), but not to B7-1 or B7-2. Here we provide in vivo genetic evidence that ICOS delivers a co-stimulatory signal that is essential both for efficient interaction between T and B cells and for normal antibody responses to T-cell-dependent antigens. To determine the physiological function of ICOS, we generated and characterized gene-targeted ICOS-deficient mice. In vivo, a lack of ICOS results in severely deficient T-cell-dependent B-cell responses. Germinal centre formation is impaired and immunoglobulin class switching, including production of allergy-mediating IgE, is defective. ICOS-deficient T cells primed in in vivo and restimulated in vitro with specific antigen produce only low levels of interleukin-4, but remain fully competent to produce interferon-gamma. 相似文献
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Ishii H Kataura H Shiozawa H Yoshioka H Otsubo H Takayama Y Miyahara T Suzuki S Achiba Y Nakatake M Narimura T Higashiguchi M Shimada K Namatame H Taniguchi M 《Nature》2003,426(6966):540-544
The electronic transport properties of conventional three-dimensional metals are successfully described by Fermi-liquid theory. But when the dimensionality of such a system is reduced to one, the Fermi-liquid state becomes unstable to Coulomb interactions, and the conduction electrons should instead behave according to Tomonaga-Luttinger-liquid (TLL) theory. Such a state reveals itself through interaction-dependent anomalous exponents in the correlation functions, density of states and momentum distribution of the electrons. Metallic single-walled carbon nanotubes (SWNTs) are considered to be ideal one-dimensional systems for realizing TLL states. Indeed, the results of transport measurements on metal-SWNT and SWNT-SWNT junctions have been attributed to the effects of tunnelling into or between TLLs, although there remains some ambiguity in these interpretations. Direct observations of the electronic states in SWNTs are therefore needed to resolve these uncertainties. Here we report angle-integrated photoemission measurements of SWNTs. Our results reveal an oscillation in the pi-electron density of states owing to one-dimensional van Hove singularities, confirming the one-dimensional nature of the valence band. The spectral function and intensities at the Fermi level both exhibit power-law behaviour (with almost identical exponents) in good agreement with theoretical predictions for the TLL state in SWNTs. 相似文献
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P S Ohashi T W Mak P Van den Elsen Y Yanagi Y Yoshikai A F Calman C Terhorst J D Stobo A Weiss 《Nature》1985,316(6029):606-609
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Haploinsufficiency of NSD1 causes Sotos syndrome 总被引:14,自引:0,他引:14
Kurotaki N Imaizumi K Harada N Masuno M Kondoh T Nagai T Ohashi H Naritomi K Tsukahara M Makita Y Sugimoto T Sonoda T Hasegawa T Chinen Y Tomita Ha HA Kinoshita A Mizuguchi T Yoshiura Ki K Ohta T Kishino T Fukushima Y Niikawa N Matsumoto N 《Nature genetics》2002,30(4):365-366
We isolated NSD1 from the 5q35 breakpoint in an individual with Sotos syndrome harboring a chromosomal translocation. We identified 1 nonsense, 3 frameshift and 20 submicroscopic deletion mutations of NSD1 among 42 individuals with sporadic cases of Sotos syndrome. The results indicate that haploinsufficiency of NSD1 is the major cause of Sotos syndrome. 相似文献
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Bourdon A Minai L Serre V Jais JP Sarzi E Aubert S Chrétien D de Lonlay P Paquis-Flucklinger V Arakawa H Nakamura Y Munnich A Rötig A 《Nature genetics》2007,39(6):776-780
Mitochondrial DNA (mtDNA) depletion syndrome (MDS; MIM 251880) is a prevalent cause of oxidative phosphorylation disorders characterized by a reduction in mtDNA copy number. The hitherto recognized disease mechanisms alter either mtDNA replication (POLG (ref. 1)) or the salvage pathway of mitochondrial deoxyribonucleosides 5'-triphosphates (dNTPs) for mtDNA synthesis (DGUOK (ref. 2), TK2 (ref. 3) and SUCLA2 (ref. 4)). A last gene, MPV17 (ref. 5), has no known function. Yet the majority of cases remain unexplained. Studying seven cases of profound mtDNA depletion (1-2% residual mtDNA in muscle) in four unrelated families, we have found nonsense, missense and splice-site mutations and in-frame deletions of the RRM2B gene, encoding the cytosolic p53-inducible ribonucleotide reductase small subunit. Accordingly, severe mtDNA depletion was found in various tissues of the Rrm2b-/- mouse. The mtDNA depletion triggered by p53R2 alterations in both human and mouse implies that p53R2 has a crucial role in dNTP supply for mtDNA synthesis. 相似文献
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Tsurusaki Y Okamoto N Ohashi H Kosho T Imai Y Hibi-Ko Y Kaname T Naritomi K Kawame H Wakui K Fukushima Y Homma T Kato M Hiraki Y Yamagata T Yano S Mizuno S Sakazume S Ishii T Nagai T Shiina M Ogata K Ohta T Niikawa N Miyatake S Okada I Mizuguchi T Doi H Saitsu H Miyake N Matsumoto N 《Nature genetics》2012,44(4):376-378
By exome sequencing, we found de novo SMARCB1 mutations in two of five individuals with typical Coffin-Siris syndrome (CSS), a rare autosomal dominant anomaly syndrome. As SMARCB1 encodes a subunit of the SWItch/Sucrose NonFermenting (SWI/SNF) complex, we screened 15 other genes encoding subunits of this complex in 23 individuals with CSS. Twenty affected individuals (87%) each had a germline mutation in one of six SWI/SNF subunit genes, including SMARCB1, SMARCA4, SMARCA2, SMARCE1, ARID1A and ARID1B. 相似文献