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Park, Ja-Young,Skonieczny, Kamil,Aratani, Naoki,Osuka, Atsuhiro,Gryko, Daniel T.,Lee, Chang-Hee The Royal Society of Chemistry 2012 Chemical communications Vol.48 No.65
<P>Calix[4]pyrroles bearing two proximally crossing straps on the same or the opposite sides have been synthesized for the first time. The doubly <I>cis</I>-strapped compound exhibited highly cooperative six-point hydrogen bonding interactions with the anion involving both pyrrolic N–Hs and Ar–Hs.</P> <P>Graphic Abstract</P><P>Calix[4]pyrroles bearing two proximally crossing straps on the same side or the opposite side have been synthesized and characterized. The <I>cis</I>-strapped compound encapsulates the fluoride anion strongly by six-point hydrogen bonding interaction while the <I>trans</I>-strapped compound shows very weak binding. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c2cc33537a'> </P>
Zhao, Ling,Kwon, Myung-Ja,Huang, Shurong,Lee, Joo Y.,Fukase, Koichi,Inohara, Naohiro,Hwang, Daniel H. American Society for Biochemistry and Molecular Bi 2007 The Journal of biological chemistry Vol.282 No.16
<P>Nucleotide-binding oligomerization domain-containing proteins (Nods) are intracellular pattern recognition receptors recognizing conserved moieties of bacterial peptidoglycan through their leucine-rich repeats domain. The agonists for Nods activate proinflammatory signaling pathways, including NF-kappaB pathways. The results from our previous studies showed that the activation of TLR4 and TLR2, leucine-rich repeat-containing pattern recognition receptors, were differentially modulated by saturated and n-3 polyunsaturated fatty acids in macrophages and dendritic cells. Here, we show the differential modulation of NF-kappaB activation and interleukin-8 (IL-8) expression in colonic epithelial cells HCT116 by saturated and unsaturated fatty acids mediated through Nods proteins. Lauric acid (C12:0) dose dependently activated NF-kappaB and induced IL-8 expression in HCT116 cells, which express both Nod1 and Nod2, but not detectable amounts of TLR2 and TLR4. These effects of lauric acid were inhibited by dominant negative forms of Nod1 or Nod2, but not by dominant negative forms of TLR2, TLR4, and TLR5. The effects of lauric acid were also attenuated by small RNA interference targeting Nod1 or Nod2. In contrast, polyunsaturated fatty acids, especially n-3 polyunsaturated fatty acids, inhibited the activation of NF-kappaB and IL-8 expression induced by lauric acid or known Nods ligands in HCT116. Furthermore, lauric acid induced, but docosahexaenoic acid inhibited lauric acid- or Nod2 ligand MDP-induced, Nod2 oligomerization in HEK293T cells transfected with Nod2. Together, these results provide new insights into the role of dietary fatty acids in modulating inflammation in colon epithelial cells. The results suggest that Nods may be involved in inducing sterile inflammation, one of the key etiological conditions in the development of many chronic inflammatory diseases.</P>
Via Method for Lithography Free Contact and Preservation of 2D Materials
Telford, Evan J.,Benyamini, Avishai,Rhodes, Daniel,Wang, Da,Jung, Younghun,Zangiabadi, Amirali,Watanabe, Kenji,Taniguchi, Takashi,Jia, Shuang,Barmak, Katayun,Pasupathy, Abhay N.,Dean, Cory R.,Hone, Ja American Chemical Society 2018 NANO LETTERS Vol.18 No.2
<P>Atomically thin 2D materials span the common components of electronic circuits as metals, semiconductors, and insulators, and can manifest correlated phases such as superconductivity, charge density waves, and magnetism. An ongoing challenge in the field is to incorporate these 2D materials into multilayer heterostructures with robust electrical contacts while preventing disorder and degradation. In particular, preserving and studying air-sensitive 2D materials has presented a significant challenge since they readily oxidize under atmospheric conditions. We report a new technique for contacting 2D materials, in which metal <I>via contacts</I> are integrated into flakes of insulating hexagonal boron nitride, and then placed onto the desired conducting 2D layer, avoiding direct lithographic patterning onto the 2D conductor. The metal contacts are planar with the bottom surface of the boron nitride and form robust contacts to multiple 2D materials. These structures protect air-sensitive 2D materials for months with no degradation in performance. This via contact technique will provide the capability to produce “atomic printed circuit boards” that can form the basis of more complex multilayer heterostructures.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/nalefd/2018/nalefd.2018.18.issue-2/acs.nanolett.7b05161/production/images/medium/nl-2017-05161z_0005.gif'></P>
Koo, Gi-Bang,Morgan, Michael J,Lee, Da-Gyum,Kim, Woo-Jung,Yoon, Jung-Ho,Koo, Ja Seung,Kim, Seung Il,Kim, Soo Jung,Son, Mi Kwon,Hong, Soon Sun,Levy, Jean M Mulcahy,Pollyea, Daniel A,Jordan, Craig T,Yan Springer Science and Business Media LLC 2015 Cell research Vol.25 No.6
<P>Receptor-interacting protein kinase-3 (RIP3 or RIPK3) is an essential part of the cellular machinery that executes 'programmed' or 'regulated' necrosis. Here we show that programmed necrosis is activated in response to many chemotherapeutic agents and contributes to chemotherapy-induced cell death. However, we show that RIP3 expression is often silenced in cancer cells due to genomic methylation near its transcriptional start site, thus RIP3-dependent activation of MLKL and downstream programmed necrosis during chemotherapeutic death is largely repressed. Nevertheless, treatment with hypomethylating agents restores RIP3 expression, and thereby promotes sensitivity to chemotherapeutics in a RIP3-dependent manner. RIP3 expression is reduced in tumors compared to normal tissue in 85% of breast cancer patients, suggesting that RIP3 deficiency is positively selected during tumor growth/development. Since hypomethylating agents are reasonably well-tolerated in patients, we propose that RIP3-deficient cancer patients may benefit from receiving hypomethylating agents to induce RIP3 expression prior to treatment with conventional chemotherapeutics.</P>