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Masahiro Fujimuro

Researcher at Kyoto Pharmaceutical University

Publications -  104
Citations -  5728

Masahiro Fujimuro is an academic researcher from Kyoto Pharmaceutical University. The author has contributed to research in topics: Primary effusion lymphoma & Kaposi's sarcoma-associated herpesvirus. The author has an hindex of 36, co-authored 93 publications receiving 5300 citations. Previous affiliations of Masahiro Fujimuro include Johns Hopkins University & University of Tokyo.

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S-nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding

TL;DR: A signalling pathway in which nitric oxide generation that follows apoptotic stimulation elicits S-nitrosylation of GAPDH, which triggers binding to Siah1 (an E3 ubiquitin ligase), nuclear translocation and apoptosis, which is prevented by NO deletion is reported.
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p53 mediates cellular dysfunction and behavioral abnormalities in Huntington's disease.

TL;DR: Evidence for a specific role of p53 in the mitochondria-associated cellular dysfunction and behavioral abnormalities of Huntington's disease is presented and findings suggest that p53 links nuclear and mitochondrial pathologies characteristic of HD.
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A novel viral mechanism for dysregulation of β-catenin in Kaposi's sarcoma–associated herpesvirus latency

TL;DR: The Kaposi's sarcoma–associated herpesvirus (KSHV) latency-associated nuclear antigen (LANA) is expressed in all KSHV-associated tumors, and it is found that β-catenin is overexpressed in both PEL cells and KS tissue.
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Production and characterization of monoclonal antibodies specific to multi-ubiquitin chains of polyubiquitinated proteins

TL;DR: A simple method was developed for the efficient preparation of polyubiquitinated proteins which are degraded by the 26 S proteasome in an ATP‐dependent manner, which enabled us to produce ten monoclonal antibodies that recognized the multi‐ubiqu itin chains of the polyubiqueinated proteins, but not free ubiquitin or the protein moieties.
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SKIP, a CBF1-associated protein, interacts with the ankyrin repeat domain of NotchIC To facilitate NotchIC function.

TL;DR: The results suggest a model in which NotchIC activates responsive promoters by competing with the SMRT-corepressor complex for contacts on both CBF1 and SKIP.