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Institution

Kyoto University

EducationKyoto, 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.


Papers
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Journal ArticleDOI
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

Book
Hiraku Nakajima1
17 Sep 1999

942 citations

Journal ArticleDOI
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

NameH-indexPapersCitations
Kari Alitalo174817114231
Ralph M. Steinman171453121518
Masayuki Yamamoto1711576123028
Karl Deisseroth160556101487
Kenji Kangawa1531117110059
Takashi Taniguchi1522141110658
Ben Zhong Tang1492007116294
Takeo Kanade147799103237
Yuji Matsuzawa143836116711
Tasuku Honjo14171288428
Kenneth M. Yamada13944672136
Y. B. Hsiung138125894278
Shuh Narumiya13759570183
Kevin P. Campbell13752160854
Junji Tojo13587884615
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023234
2022679
20218,533
20208,740
20198,050
20187,932