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Harimoto, H.

Publications and source records attributed to Harimoto, H..

2 recordsLinked to original sources

Identification of novel ubiquitin receptors on the 26S proteasome by photo-crosslinking mass spectrometry

The 26S proteasome is the endpoint of the ubiquitin-proteasome system, an essential pathway for maintaining cellular homeostasis through targeted degradation of misfolded, damaged, and obsolete proteins. Substrates labeled with ubiquitin are directed to the 26S proteasome by binding to one or more ubiquitin receptors. However, ubiquitin-dependent degradation occurs even when the canonical receptor sites are mutated, suggesting the presence of additional, unidentified binding sites. Here we created photo-crosslinkable probes for ubiquitin interactions by incorporating the unnatural amino acid p-benzoyl-L-phenylalanine into ubiquitin. We show that these probes can be used to measure apparent affinities for known receptors and to reveal novel ubiquitin-binding sites on the yeast 26S proteasome. Through photo-crosslinking mass-spectrometry experiments we identified a groove on the top of the proteasome, formed by Rpn2, Rpn9, Rpn10, and Rpn12, that serves as an additional ubiquitin-binding interface. Our photo-crosslinkable probes thus serve as versatile tools for the characterization of ubiquitin-protein interactions and the identification of ubiquitin-binding domains.

biochemistry↗

Anti-CD137 monoclonal antibody enhances trastuzumab-induced, natural killer cell-mediated cytotoxicity against pancreatic cancer cell lines with low human epidermal growth factor-like receptor 2 expression

BackgroundBecause human epidermal growth factor-like receptor (HER) 2 is expressed on the surface of human pancreatic carcinoma cells to varying degrees, trastuzumab, an anti-HER2 monoclonal antibody (mAb), is expected to exert antibody-dependent, natural killer (NK) cell-mediated cytotoxicity (ADCC) against the cells. However, some reports found that the effect of trastuzumab against human pancreatic carcinoma cells was limited because most express only limited HER2.\n\nMethodsWe examined whether anti-CD137 stimulating mAb could enhance trastuzumab-mediated ADCC against Panc-1, a human pancreatic cancer cell line with low HER2 expression, in vitro.\n\nResultsSupplementation of anti-CD137 mAb could improve trastuzumab-mediated ADCC against Panc-1 which was insufficient without this stimulating antibody. The ADCC differed in individual cells, and this was related to the expression of CD137 on the surface of NK cells after trastuzumab stimulation in association with the Fc{gamma}-RIIIA polymorphism. NK cells with Fc{gamma}-RIIIA-VV/VF showed high levels of ADCC against Panc-1, but those with Fc{gamma}-RIIIA-FF did not show optimal ADCC. In addition, trastuzumab-mediated ADCC against the human pancreatic cancer cell line Capan-1 with high HER2 expression was generally high and not affected by the Fc{gamma}-RIIIA polymorphism.\n\nConclusionsThese results demonstrated that in Fc{gamma}-RIIIA-VV/VF-carrying hosts, trastuzumab plus CD137 mAb could induce effective ADCC against HER2-low-expressing pancreatic cancer cells. This also indicates the therapeutic potential for unresectable human pancreatic cancer, in which HER-2 expression is generally low.

immunology↗