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  • 1
    Publication Date: 2011-06-21
    Description: Author(s): LiDong Pan and C. C. Huang Null transmission ellipsometry was employed to study the temperature evolution of the helical structure of the smectic- C α * phase. Free-standing films with thickness ranging from 31 to more than 400 layers were prepared and studied. The experimental results show a reduced twisting power in thin films... [Phys. Rev. E 83, 060702] Published Mon Jun 20, 2011
    Keywords: Liquid crystals
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 2
    Publication Date: 2011-06-15
    Description: Author(s): LiDong Pan, B. K. McCoy, Shun Wang, Z. Q. Liu, S. T. Wang, R. Pindak, and C. C. Huang Null transmission ellipsometry and resonant x-ray diffraction are employed to study the effect of enantiomeric excess (EE) on the phase behavior of antiferroelectric liquid crystal 10OTBBB1M7. Phase sequence, layer spacing, and pitch of the helical structures of the smectic- C α * and smectic- C * phases... [Phys. Rev. E 83, 060701] Published Tue Jun 14, 2011
    Keywords: Liquid crystals
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 3
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    American Physical Society (APS)
    Publication Date: 2011-11-10
    Description: Author(s): LiDong Pan and C. C. Huang [Phys. Rev. E 84, 051703] Published Wed Nov 09, 2011
    Keywords: Liquid crystals
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
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  • 4
    Publication Date: 2012-12-29
    Description: Author(s): Y. Sasaki, K. V. Le, S. Aya, M. Isobe, H. Yao, C. C. Huang, H. Takezoe, and K. Ema We carried out an improved characterization of phase transitions among chiral smectic- C subphases observed for various antiferroelectric liquid crystals by precise heat capacity measurements. It was found that the phase transitions are intrinsically first order exhibiting a remarkable heat anomaly w... [Phys. Rev. E 86, 061704] Published Fri Dec 28, 2012
    Keywords: Liquid crystals
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 5
    Publication Date: 2011-07-15
    Description: Author(s): C. L. Folcia, J. Ortega, J. Etxebarria, LiDong Pan, Shun Wang, C. C. Huang, V. Ponsinet, P. Barois, R. Pindak, and N. Gimeno We report structural results that evidence the polarization distribution of the blocks in the columnar phase of an achiral bent-core liquid crystal. The study was performed using resonant x-ray diffraction at the sulfur K edge on oriented samples aligned on substrates. The extra periodicity is revea... [Phys. Rev. E 84, 010701] Published Thu Jul 14, 2011
    Keywords: Liquid crystals
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 6
    Publication Date: 2011-07-16
    Description: Author(s): V. Ponsinet, P. Barois, LiDong Pan, Shun Wang, C. C. Huang, S. T. Wang, R. Pindak, U. Baumeister, and W. Weissflog The chiral antiferroelectric structure of an achiral bent-core liquid crystal is characterized by resonant x-ray scattering at chlorine K edge. The “forbidden” reflections resulting from the glide or screw symmetry elements are restored by the anisotropy of the tensor structure factor, which we calc... [Phys. Rev. E 84, 011706] Published Fri Jul 15, 2011
    Keywords: Liquid crystals
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 7
    Publication Date: 2001-09-08
    Description: Bcl-2 family members bearing only the BH3 domain are essential inducers of apoptosis. We identified a BH3-only protein, Bmf, and show that its BH3 domain is required both for binding to prosurvival Bcl-2 proteins and for triggering apoptosis. In healthy cells, Bmf is sequestered to myosin V motors by association with dynein light chain 2. Certain damage signals, such as loss of cell attachment (anoikis), unleash Bmf, allowing it to translocate and bind prosurvival Bcl-2 proteins. Thus, at least two mammalian BH3-only proteins, Bmf and Bim, function to sense intracellular damage by their localization to distinct cytoskeletal structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puthalakath, H -- Villunger, A -- O'Reilly, L A -- Beaumont, J G -- Coultas, L -- Cheney, R E -- Huang, D C -- Strasser, A -- CA 80188/CA/NCI NIH HHS/ -- R29 DC003299/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2001 Sep 7;293(5536):1829-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne, P.O. Royal Melbourne Hospital, 3050 VIC, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11546872" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Anoikis ; Apoptosis Regulatory Proteins ; Calmodulin-Binding Proteins/*metabolism ; Carrier Proteins/*chemistry/genetics/*metabolism ; Cell Line ; Cytoskeleton/metabolism ; *Drosophila Proteins ; Dyneins ; Gene Expression Profiling ; Humans ; *Membrane Proteins ; Mice ; Molecular Motor Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; *Myosin Type V ; Neoplasm Proteins/genetics/metabolism ; Nerve Tissue Proteins/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Protein Transport ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2/chemistry/genetics/metabolism ; RNA, Messenger/analysis/genetics ; Transfection ; Two-Hybrid System Techniques
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2009-07-25
    Description: FAS (also called APO-1 and CD95) and its physiological ligand, FASL, regulate apoptosis of unwanted or dangerous cells, functioning as a guardian against autoimmunity and cancer development. Distinct cell types differ in the mechanisms by which the 'death receptor' FAS triggers their apoptosis. In type I cells, such as lymphocytes, activation of 'effector caspases' by FAS-induced activation of caspase-8 suffices for cell killing, whereas in type II cells, including hepatocytes and pancreatic beta-cells, caspase cascade amplification through caspase-8-mediated activation of the pro-apoptotic BCL-2 family member BID (BH3 interacting domain death agonist) is essential. Here we show that loss of XIAP (X-chromosome linked inhibitor of apoptosis protein) function by gene targeting or treatment with a second mitochondria-derived activator of caspases (SMAC, also called DIABLO; direct IAP-binding protein with low pI) mimetic drug in mice rendered hepatocytes and beta-cells independent of BID for FAS-induced apoptosis. These results show that XIAP is the critical discriminator between type I and type II apoptosis signalling and suggest that IAP inhibitors should be used with caution in cancer patients with underlying liver conditions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2956120/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2956120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jost, Philipp J -- Grabow, Stephanie -- Gray, Daniel -- McKenzie, Mark D -- Nachbur, Ueli -- Huang, David C S -- Bouillet, Philippe -- Thomas, Helen E -- Borner, Christoph -- Silke, John -- Strasser, Andreas -- Kaufmann, Thomas -- CA 43540/CA/NCI NIH HHS/ -- CA 80188/CA/NCI NIH HHS/ -- R01 CA043540/CA/NCI NIH HHS/ -- R01 CA043540-09/CA/NCI NIH HHS/ -- R01 CA043540-22/CA/NCI NIH HHS/ -- R01 CA080188-01/CA/NCI NIH HHS/ -- R01 CA080188-08/CA/NCI NIH HHS/ -- England -- Nature. 2009 Aug 20;460(7258):1035-9. doi: 10.1038/nature08229. Epub 2009 Jul 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne University, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19626005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/antagonists & inhibitors/immunology/*metabolism ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein/deficiency/genetics ; Biomimetic Materials/pharmacology ; Caspase Inhibitors ; Enzyme Activation ; Fas Ligand Protein/metabolism ; Female ; Hepatitis/metabolism/pathology ; Hepatocytes/cytology/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Signal Transduction ; Thymus Gland/cytology/drug effects ; X-Linked Inhibitor of Apoptosis Protein/antagonists & ; inhibitors/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2007-02-10
    Description: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2012-09-01
    Description: The mammalian circadian clock involves a transcriptional feed back loop in which CLOCK and BMAL1 activate the Period and Cryptochrome genes, which then feedback and repress their own transcription. We have interrogated the transcriptional architecture of the circadian transcriptional regulatory loop on a genome scale in mouse liver and find a stereotyped, time-dependent pattern of transcription factor binding, RNA polymerase II (RNAPII) recruitment, RNA expression, and chromatin states. We find that the circadian transcriptional cycle of the clock consists of three distinct phases: a poised state, a coordinated de novo transcriptional activation state, and a repressed state. Only 22% of messenger RNA (mRNA) cycling genes are driven by de novo transcription, suggesting that both transcriptional and posttranscriptional mechanisms underlie the mammalian circadian clock. We also find that circadian modulation of RNAPII recruitment and chromatin remodeling occurs on a genome-wide scale far greater than that seen previously by gene expression profiling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694775/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694775/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koike, Nobuya -- Yoo, Seung-Hee -- Huang, Hung-Chung -- Kumar, Vivek -- Lee, Choogon -- Kim, Tae-Kyung -- Takahashi, Joseph S -- F32 DA024556/DA/NIDA NIH HHS/ -- R01 NS053616/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):349-54. doi: 10.1126/science.1226339. Epub 2012 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936566" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Chromatin/*metabolism ; Chromatin Assembly and Disassembly/genetics ; Circadian Clocks/*genetics ; Cryptochromes/*genetics ; DNA, Intergenic ; Enhancer Elements, Genetic ; *Epigenesis, Genetic ; Gene Expression Profiling ; Genetic Loci ; Histones/metabolism ; Liver/metabolism/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Period Circadian Proteins/genetics ; RNA Polymerase II/metabolism ; RNA, Messenger/genetics ; *Transcription, Genetic ; *Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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