Institution
Kyoto University
Education•Kyoto, Japan•
About: Kyoto University is a education organization based out in Kyoto, Japan. It is known for research contribution in the topics: Population & Catalysis. The organization has 85837 authors who have published 217215 publications receiving 6526826 citations. The organization is also known as: Kyōto University & Kyōto daigaku.
Topics: Population, Catalysis, Transplantation, Polymerization, Gene
Papers published on a yearly basis
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942 citations
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TL;DR: The XIS is an X-ray imaging spectrometer system, consisting of state-of-the-art charge-coupled devices (CCDs) optimized for Xray detection, camera bodies, and control electronics as mentioned in this paper.
Abstract: The XIS is an X-ray Imaging Spectrometer system, consisting of state-of-the-art charge-coupled devices (CCDs) optimized for X-ray detection, camera bodies, and control electronics. Four sets of XIS sensors are placed at the focal planes of the grazing-incidence, nested thin-foil mirrors (XRT: X-Ray Telescope) onboard the Suzaku satellite. Three of the XIS sensors have front-illuminated CCDs, while the other has a back-illuminated CCD. Coupled with the XRT, the energy range of 0.2–12keV with energy resolution of 130eV at 5.9keV, and a field of view of 18 � ×18 �
942 citations
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TL;DR: This integrated molecular analysis of clear-cell renal cell carcinoma unmasked new correlations between DNA methylation, gene mutation and/or gene expression and copy number profiles, enabling the stratification of clinical risks for patients with ccRCC.
Abstract: Clear-cell renal cell carcinoma (ccRCC) is the most prevalent kidney cancer and its molecular pathogenesis is incompletely understood. Here we report an integrated molecular study of ccRCC in which ≥100 ccRCC cases were fully analyzed by whole-genome and/or whole-exome and RNA sequencing as well as by array-based gene expression, copy number and/or methylation analyses. We identified a full spectrum of genetic lesions and analyzed gene expression and DNA methylation signatures and determined their impact on tumor behavior. Defective VHL-mediated proteolysis was a common feature of ccRCC, which was caused not only by VHL inactivation but also by new hotspot TCEB1 mutations, which abolished Elongin C-VHL binding, leading to HIF accumulation. Other newly identified pathways and components recurrently mutated in ccRCC included PI3K-AKT-mTOR signaling, the KEAP1-NRF2-CUL3 apparatus, DNA methylation, p53-related pathways and mRNA processing. This integrated molecular analysis unmasked new correlations between DNA methylation, gene mutation and/or gene expression and copy number profiles, enabling the stratification of clinical risks for patients with ccRCC.
938 citations
Authors
Showing all 86225 results
Name | H-index | Papers | Citations |
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Kari Alitalo | 174 | 817 | 114231 |
Ralph M. Steinman | 171 | 453 | 121518 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Karl Deisseroth | 160 | 556 | 101487 |
Kenji Kangawa | 153 | 1117 | 110059 |
Takashi Taniguchi | 152 | 2141 | 110658 |
Ben Zhong Tang | 149 | 2007 | 116294 |
Takeo Kanade | 147 | 799 | 103237 |
Yuji Matsuzawa | 143 | 836 | 116711 |
Tasuku Honjo | 141 | 712 | 88428 |
Kenneth M. Yamada | 139 | 446 | 72136 |
Y. B. Hsiung | 138 | 1258 | 94278 |
Shuh Narumiya | 137 | 595 | 70183 |
Kevin P. Campbell | 137 | 521 | 60854 |
Junji Tojo | 135 | 878 | 84615 |