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  • 1
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    Debris-carrying camouflage among diverse lineages of Cretaceous insects (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-06-25
    Description: Insects have evolved diverse methods of camouflage that have played an important role in their evolutionary success. Debris-carrying, a behavior of actively harvesting and carrying exogenous materials, is among the most fascinating and complex behaviors because it requires not only an ability to recognize, collect, and carry materials but also evolutionary adaptations in related morphological characteristics. However, the fossil record of such behavior is extremely scarce, and only a single Mesozoic example from Spanish amber has been recorded; therefore, little is known about the early evolution of this complicated behavior and its underlying anatomy. We report a diverse insect assemblage of exceptionally preserved debris carriers from Cretaceous Burmese, French, and Lebanese ambers, including the earliest known chrysopoid larvae (green lacewings), myrmeleontoid larvae (split-footed lacewings and owlflies), and reduviids (assassin bugs). These ancient insects used a variety of debris material, including insect exoskeletons, sand grains, soil dust, leaf trichomes of gleicheniacean ferns, wood fibers, and other vegetal debris. They convergently evolved their debris-carrying behavior through multiple pathways, which expressed a high degree of evolutionary plasticity. We demonstrate that the behavioral repertoire, which is associated with considerable morphological adaptations, was already widespread among insects by at least the Mid-Cretaceous. Together with the previously known Spanish specimen, these fossils are the oldest direct evidence of camouflaging behavior in the fossil record. Our findings provide a novel insight into early evolution of camouflage in insects and ancient ecological associations among plants and insects.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Complex I assembly function and fatty acid oxidation enzyme activity of ACAD9 both contribute to disease severity in ACAD9 deficiency (2015)
    Oxford University Press
    Details
    Publication Date: 2015-05-09
    Description: Acyl-CoA dehydrogenase 9 (ACAD9) is an assembly factor for mitochondrial respiratory chain Complex I (CI), and ACAD9 mutations are recognized as a frequent cause of CI deficiency. ACAD9 also retains enzyme ACAD activity for long-chain fatty acids in vitro , but the biological relevance of this function remains controversial partly because of the tissue specificity of ACAD9 expression: high in liver and neurons and minimal in skin fibroblasts. In this study, we hypothesized that this enzymatic ACAD activity is required for full fatty acid oxidation capacity in cells expressing high levels of ACAD9 and that loss of this function is important in determining phenotype in ACAD9-deficient patients. First, we confirmed that HEK293 cells express ACAD9 abundantly. Then, we showed that ACAD9 knockout in HEK293 cells affected long-chain fatty acid oxidation along with Cl, both of which were rescued by wild type ACAD9 . Further, we evaluated whether the loss of ACAD9 enzymatic fatty acid oxidation affects clinical severity in patients with ACAD9 mutations. The effects on ACAD activity of 16 ACAD9 mutations identified in 24 patients were evaluated using a prokaryotic expression system. We showed that there was a significant inverse correlation between residual enzyme ACAD activity and phenotypic severity of ACAD9-deficient patients. These results provide evidence that in cells where it is strongly expressed, ACAD9 plays a physiological role in fatty acid oxidation, which contributes to the severity of the phenotype in ACAD9-deficient patients. Accordingly, treatment of ACAD9 patients should aim at counteracting both CI and fatty acid oxidation dysfunctions.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 3
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    Large Exchange Bias after Zero-Field Cooling from an Unmagnetized State (2011)
    American Physical Society (APS)
    Details
    Publication Date: 2011-02-18
    Description: Author(s): B. M. Wang, Y. Liu, P. Ren, B. Xia, K. B. Ruan, J. B. Yi, J. Ding, X. G. Li, and L. Wang Exchange bias (EB) is usually observed in systems with an interface between different magnetic phases after field cooling. Here we report an unusual phenomenon in which a large EB can be observed in Ni-Mn-In bulk alloys after zero-field cooling from an unmagnetized state. We propose that this is rel... [Phys. Rev. Lett. 106, 077203] Published Thu Feb 17, 2011
    Keywords: Condensed Matter: Electronic Properties, etc.
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
    Published by American Physical Society (APS)
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  • 4
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    U1 snRNP is mislocalized in ALS patient fibroblasts bearing NLS mutations in FUS and is required for motor neuron outgrowth in zebrafish (2015)
    Oxford University Press
    Details
    Publication Date: 2015-04-02
    Description: Mutations in FUS cause amyotrophic lateral sclerosis (ALS), but the molecular pathways leading to neurodegeneration remain obscure. We previously found that U1 snRNP is the most abundant FUS interactor. Here, we report that components of the U1 snRNP core particle (Sm proteins and U1 snRNA), but not the mature U1 snRNP-specific proteins (U1-70K, U1A and U1C), co-mislocalize with FUS to the cytoplasm in ALS patient fibroblasts harboring mutations in the FUS nuclear localization signal (NLS). Similar results were obtained in HeLa cells expressing the ALS-causing FUS R495X NLS mutation, and mislocalization of Sm proteins is RRM-dependent. Moreover, as observed with FUS, knockdown of any of the U1 snRNP-specific proteins results in a dramatic loss of SMN-containing Gems. Significantly, knockdown of U1 snRNP in zebrafish results in motor axon truncations, a phenotype also observed with FUS, SMN and TDP-43 knockdowns. Our observations linking U1 snRNP to ALS patient cells with FUS mutations, SMN-containing Gems, and motor neurons indicate that U1 snRNP is a component of a molecular pathway associated with motor neuron disease. Linking an essential canonical splicing factor (U1 snRNP) to this pathway provides strong new evidence that splicing defects may be involved in pathogenesis and that this pathway is a potential therapeutic target.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 5
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    SUMOylation deregulates tau degradation [Neuroscience] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-11-19
    Description: Intracellular accumulation of the abnormally modified tau is hallmark pathology of Alzheimer’s disease (AD), but the mechanism leading to tau aggregation is not fully characterized. Here, we studied the effects of tau SUMOylation on its phosphorylation, ubiquitination, and degradation. We show that tau SUMOylation induces tau hyperphosphorylation at multiple AD-associated...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    RAP80 targets BRCA1 to specific ubiquitin structures at DNA damage sites (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: Mutations affecting the BRCT domains of the breast cancer-associated tumor suppressor BRCA1 disrupt the recruitment of this protein to DNA double-strand breaks (DSBs). The molecular structures at DSBs recognized by BRCA1 are presently unknown. We report the interaction of the BRCA1 BRCT domain with RAP80, a ubiquitin-binding protein. RAP80 targets a complex containing the BRCA1-BARD1 (BRCA1-associated ring domain protein 1) E3 ligase and the deubiquitinating enzyme (DUB) BRCC36 to MDC1-gammaH2AX-dependent lysine(6)- and lysine(63)-linked ubiquitin polymers at DSBs. These events are required for cell cycle checkpoint and repair responses to ionizing radiation, implicating ubiquitin chain recognition and turnover in the BRCA1-mediated repair of DSBs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706583/" 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/PMC2706583/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sobhian, Bijan -- Shao, Genze -- Lilli, Dana R -- Culhane, Aedin C -- Moreau, Lisa A -- Xia, Bing -- Livingston, David M -- Greenberg, Roger A -- K08 CA106597/CA/NCI NIH HHS/ -- K08 CA106597-01A2/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1198-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Genetics and Department of Medicine, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525341" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; BRCA1 Protein/*metabolism ; Binding Sites ; Carrier Proteins/*metabolism ; Cell Line ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair/physiology ; HeLa Cells ; Humans ; Mice ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Nucleic Acid Conformation ; Protein Structure, Tertiary ; Tumor Suppressor Proteins/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligases/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Analysis of economic efficiency and eco-efficiency of Chinese star hotels based on SBM model (2018)
    Institute of Physics (IOP)
    Details
    Publication Date: 2018-10-31
    Description: Star hotels, as the core sector of China’s tourism development, the improvement of their economic efficiency is an important way for the tourism industry to operate well. On the other hand, improving eco-efficiency can promote star hotels to take more responsibility for the ecological environment and promote the sustainable development of tourism industry. In this paper, the A Slacks-Based Measure model (SBM), as one kind of data envelopment analysis, is used to construct the economic efficiency and eco efficiency input-output system of Chinese star hotels according to the development characteristics of star hotels in China. By collecting the data in 2014 and using the energy balance sheet to calculate the carbon emission, we further calculate the economic efficiency and eco-efficiency level of the star hotels in 30 provinces in China’s main land, and further analysis the input-output spatial pattern and development trend of the eco-economic system in China’s star hotels through...
    Print ISSN: 1755-1307
    Electronic ISSN: 1755-1315
    Topics: Geography , Geosciences , Physics
    Published by Institute of Physics (IOP)
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  • 8
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    Development patterns and cooperation paths of tourism industry within the China–Mongolia–Russia Economic Corridor (2018)
    Institute of Physics (IOP)
    Details
    Publication Date: 2018-10-31
    Description: Strengthening tourism cooperation in border areas along the China–Mongolia–Russia Economic Corridor (CMREC) are important and challenging, under “Belt and Road” (B&R) initiative. Research has constructed a tourism competitiveness evaluation model including three dimensions and based on six factors: natural resources, cultural resources, tourism market, social economy, traffic facilities, and policy support. The results show the spatial characteristics of tourism competitiveness ordered as Beijing–Tianjin–Hebei of China, Northeast China, Northwest China, Russian Siberia Federal District, Mongolia, Russian Far East Federal District, and Russian Ural Federal District. Data show that the average tourism competitiveness of the three areas in Northern China are 2.69 times those of the three Russian areas, and 1.74 times those of Mongolia; at the same time, the average tourism competitiveness of Mongolia is 1.54 times that of the three areas of Russia. Based on the evaluation resul...
    Print ISSN: 1755-1307
    Electronic ISSN: 1755-1315
    Topics: Geography , Geosciences , Physics
    Published by Institute of Physics (IOP)
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  • 9
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    A function for cyclin D1 in DNA repair uncovered by protein interactome analyses in human cancers (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-06-10
    Description: Cyclin D1 is a component of the core cell cycle machinery. Abnormally high levels of cyclin D1 are detected in many human cancer types. To elucidate the molecular functions of cyclin D1 in human cancers, we performed a proteomic screen for cyclin D1 protein partners in several types of human tumours. Analyses of cyclin D1 interactors revealed a network of DNA repair proteins, including RAD51, a recombinase that drives the homologous recombination process. We found that cyclin D1 directly binds RAD51, and that cyclin D1-RAD51 interaction is induced by radiation. Like RAD51, cyclin D1 is recruited to DNA damage sites in a BRCA2-dependent fashion. Reduction of cyclin D1 levels in human cancer cells impaired recruitment of RAD51 to damaged DNA, impeded the homologous recombination-mediated DNA repair, and increased sensitivity of cells to radiation in vitro and in vivo. This effect was seen in cancer cells lacking the retinoblastoma protein, which do not require D-cyclins for proliferation. These findings reveal an unexpected function of a core cell cycle protein in DNA repair and suggest that targeting cyclin D1 may be beneficial also in retinoblastoma-negative cancers which are currently thought to be unaffected by cyclin D1 inhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134411/" 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/PMC3134411/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jirawatnotai, Siwanon -- Hu, Yiduo -- Michowski, Wojciech -- Elias, Joshua E -- Becks, Lisa -- Bienvenu, Frederic -- Zagozdzon, Agnieszka -- Goswami, Tapasree -- Wang, Yaoyu E -- Clark, Alan B -- Kunkel, Thomas A -- van Harn, Tanja -- Xia, Bing -- Correll, Mick -- Quackenbush, John -- Livingston, David M -- Gygi, Steven P -- Sicinski, Piotr -- P01 CA080111/CA/NCI NIH HHS/ -- P01 CA080111-12/CA/NCI NIH HHS/ -- P01 CA109901/CA/NCI NIH HHS/ -- P01 CA109901-07/CA/NCI NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01 CA083688/CA/NCI NIH HHS/ -- R01 CA083688-10/CA/NCI NIH HHS/ -- R01 CA138804/CA/NCI NIH HHS/ -- R01 CA138804-02/CA/NCI NIH HHS/ -- Z01 ES065089-11/Intramural NIH HHS/ -- England -- Nature. 2011 Jun 8;474(7350):230-4. doi: 10.1038/nature10155.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654808" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Comet Assay ; Cyclin D1/deficiency/*metabolism ; DNA Damage/radiation effects ; *DNA Repair/radiation effects ; HeLa Cells ; Humans ; Mice ; Neoplasms/genetics/*metabolism/pathology ; Protein Binding/radiation effects ; *Protein Interaction Mapping ; Rad51 Recombinase/*metabolism ; Radiation, Ionizing ; Recombination, Genetic/genetics ; Retinoblastoma Protein/deficiency
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Conserved regulatory elements in AMPK (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-06-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Lei -- Xin, Feng-Jiao -- Wang, Jue -- Hu, Jicheng -- Zhang, Yuan-Yuan -- Wan, Shuo -- Cao, Lu-Sha -- Lu, Chang -- Li, Peng -- Yan, S Frank -- Neumann, Dietbert -- Schlattner, Uwe -- Xia, Bin -- Wang, Zhi-Xin -- Wu, Jia-Wei -- England -- Nature. 2013 Jun 13;498(7453):E8-10. doi: 10.1038/nature12189.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MOE Key Laboratory of Protein Sciences and Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23765502" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*chemistry/*metabolism ; Adenosine Diphosphate/*metabolism/*pharmacology ; Animals
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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