1,196 research outputs found
Poly[2,7-(9,9-dihexylfluorene)]-block-poly[3-(trimethoxysilyl)propyl methacrylate] (PF-b-PTMSPMA) rod-coil block copolymers: Synthesis, morphology and photophysical properties in mixed solvents
No full textUsing Path analysis to examine causal relationships among balanced scorecard performance indicators for general hospitals: the case of a public hospital system in Taiwan
No full textLetter from Wong Puey Tung, San Hop Company to Mr. Geo. [George] H. Hand, Chief Engineer, Dominguez Estate Company, January 17, 1925
No full textResponse to letter from Hand requesting information about the employment status of Chinese individuals on land leased by Tung. Tung confirms persons are employees of his and are not breaking the Alien Land Act
Clinical improvement following home parenteral nutrition in pediatric patients with intestinal failure.
No full textLiving Anionic Polymerization of Styrene Derivatives para-Substituted with pi-Conjugated Oligo(fluorene) Moieties
No full text
WHY HAS THE PAPER ENTITLED "GREATWALL-PHOSPHORYLATED Α-ENDOSULFINE IS BOTH AN INHIBITOR AND A SUBSTRATE OF PP2A-B55 HETEROTRIMERS" BY WILLIAMS, M.C. ET AL. THAT WAS PUBLISHED IN ELIFE [WILLIAMS, B.C., FILTER, J.J., BLAKE-HODEK, K.A., FUDA, N.J., SHALLOWAY, D. AND GOLDBERG, M.L. (2014) ELIFE, DOI: 10.7554/ELIFE.01695 ] NOT BEEN RETRACTED?
No full textThe paper entitled "Greatwall-phosphorylated α-Endosulfine is both an inhibitor and a substrate of PP2A-B55 heterotrimers" authored by Williams, B.C. et al. [Williams, B.C., Filter, J.J., Blake-Hodek, K.A., Fuda, N.J., Shalloway, D. and Goldberg, M.L. and Published in the Journal eLife [eLife (2014) e01695, doi: 10.7554/elife.01695] was the subject of an investigative critique [Tung, H.Y.L. (2020) J. Invest. Cri. Pub. Sci. Articles, Vol. 1, pp193-200, DOI: 10.5281/zenodo.5115188]. It was previously reported that the paper by Williams, et al. was riddled with Dishonest Scientific Reported, Data Falsification and possibly Data Fabrication. After, contacting the Editor in Chief of eLife, Drs Michael B. Eisen, the author of this report was referred to the Managing Editor of eLife, Dr Wei Mun Chan who is not an expert in Enzymology by any stretch of imagination. The Managing Editor of eLife apparently obtained some response from Williams, et al. which was not only unsatisfactory scientifically but aggravated the seriousness of this case as it was revealed that Williams et al. obtained conclusions of their paper based on some experiments in which they were counting ~3 cpm of radioactivity above background. When the author of this report pointed the fantastical results that Williams et al. claimed they were able to obtain, the author of this Report received no sign of life from the Managing editor and the Editor in Chief of eLife. This Report provides further evidence that Williams, B.C. et al. committed Dishonest Scientific Reporting, Data Falsification and Data Fabrication in their paper
International Trade Law and Information Policy: A Recent History
No full textBy looking at the practices of both the United States Trade Representative and selected international treaty-making bodies, this paper explores the origins of the current conflict over information access in trade diplomacy and identifies what these trends may portend for information access regarding future agreements
Academic Law Libraries and the Crisis in Legal Education
No full textToday's law schools are threatened by declining enrollments and poor job prospects for graduates. Prominent reformers are exposing dysfunctions within the current system and recommending improvements, but many of these proposals misunderstand academic law libraries and their contributions to student and faculty success. This article examines four possible curricular reforms and suggests ways that law librarians can participate in an comprehensive effort to make legal education more useful
YC-1 inhibits proliferation of breast cancer cells by down-regulating EZH2 expression via activation of c-Cbl and ERK
No full textBACKGROUND AND PURPOSE
YC-1 exhibits potent anticancer activity via numerous actions in many cancer cell lines. Hence, we investigated the in vivo antitumour efficacy of YC-1 in an MDA-MB-468 xenograft model and elucidated the mechanism of down-regulation of enhancer of zeste homology 2 (EZH2) by YC-1 in breast cancer cells.
EXPERIMENTAL APPROACH
In YC-1-treated breast cancer cells and tumour specimens from YC-1-treated MDA-MB-468 xenografts, EZH2 expression was analysed by Western blotting. Pharmacological inhibitors and short hairpin RNA-mediated knockdown were applied to identify possible signalling pathways involved in EZH2 down-regulation by YC-1.
KEY RESULTS
YC-1 reduced the viability of breast cancer cells and tumour growth in MDA-MB-468 xenografts. In breast cancer cells, YC-1 down-regulated EZH2 expression in a concentration-and time-dependent manner. Depletion of EZH2 reduced the proliferation and susceptibility of breast cancer cells to YC-1-induced apoptosis. EZH2 expression was suppressed in tumour specimens from YC-1-treated MDA-MB-468 xenograft mice. YC-1 enhanced both the degradation rate and ubiquitination of EZH2. The down-regulation of EZH2 by YC-1 was associated with activation of PKA and Src-Raf-ERK-mediated signalling pathways. Furthermore, depletion of Casitas B-lineage lymphoma (c-Cbl), an E3 ubiquitin ligase, abolished YC-1-induced apoptosis and suppression of EZH2. YC-1 rapidly activated c-Cbl to induce signalling associated with ERK and EZH2.
CONCLUSION AND IMPLICATIONS
We discovered that YC-1 induces apoptosis and inhibits tumour growth of breast cancer cells via down-regulation of EZH2 by activating c-Cbl and ERK. These data suggest that YC-1 is a potential anticancer drug candidate for triple-negative breast cancer
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